In setting out to defend a more reasonable conception of genetic determinism, it is first necessary to be clear about what that conception posits. Revised genetic determinism is qualified with respect to both the traits/outcomes and individuals to which it applies and the causal power that it ascribes to genetic factors. Moreover, it does not make claims about the degree to which traits/outcomes are “caused by” genetic factors, but rather about the degree to which trait/outcome variation is under genetic control, and does not claim that variation in all traits/outcomes is mostly under genetic control. It would be absurd to argue that heredity is the primary determinant of differences in all human behavioral traits/outcomes, since some of these, e.g., short-term memory, exhibit almost no heritability, i.e., interindividual trait/outcome variation due to interindividual genetic variation (Woodley of Menie and Fernandes 2015). Further, revised genetic determinism applies only to adult humans, given that the heritability of at least some behavioral (and other) traits/outcomes rises into adulthood. Thus revised genetic determinism maintains only that variation among adults in certain significant behavioral traits/outcomes is primarily genetically determined, those being general intelligence, executive functions (i.e., cognitive controls of behavior), life history speed, and social status. (This is not to imply that there are no other important behavioral traits/outcomes variation in which is substantially genetically determined; rather, it is simply taken to be part of the definition of revised genetic determinism that it only concerns the four traits/outcomes just listed, a choice explained in the following.)

The focus is on these traits/outcomes because they are so widely believed to be extremely important for the quality of human lives, which is why research on them has generated so much controversy in the behavioral sciences (the case of general intelligence, mentioned above, is illustrative here). Whether and to what degree, say, differences in individual preferences for ice cream flavor are genetically determined is not an issue on which anything meaningful seems to hang. But it is of obviously profound importance whether and to what degree variation in general intelligence is genetically determined, since this trait substantially influences a number of critical life outcomes (Strenze 2015), e.g., educational attainment, and because the extent to which differences in it are malleable carries a number of major implications for social policy. Therefore, the fact that the ambit of revised genetic determinism is quite narrowly circumscribed barely reduces the importance of its claims relative to original genetic determinism.

With preceding sections of this entry in mind, it should be apparent that revised genetic determinism does not hold that genetic factors are the exclusive determinants of variation in any human behavioral trait/outcome (there is not sufficient evidence to support the belief that individual differences in any such trait/outcome are fully genetically determined at this point in time, at least). When writing about the greater relative contribution of genetic as opposed to (nongenetic) environmental influences to differences in behavioral phenotypes and outcomes, terms such as “primarily,” rather than “entirely” or “completely,” are therefore used.

A point that merits emphasis and elaboration is that revised genetic determinism is concerned with the degree to which trait/outcome variation is genetically determined, not the degree to which traits/outcomes are “caused by” genetic factors. It is unclear whether the latter issue will ever be elucidated. In discussions of the relative effects of genes and environmental factors on phenotypic development, it is often remarked that without “environmental input,” a genome would only make a “damp spot on the carpet” (quoted in Sesardic 2005, p. 14). This statement suggests the obvious point that neither genes nor environmental factors are in isolation sufficient to produce a phenotype. Indeed, given their interdependency, it is no clearer whether genes or environments contribute more to the development of some phenotype than it is whether kerosene or sparks contribute more to a fire resulting from their interaction, a matter that quickly leads to probably irresolvable philosophical debates about the nature of causation itself. Moreover, it is apparent that what is at issue in controversies surrounding “genetic determinism” has nothing to do with the overall degree to which a trait/outcome is “caused by” genetic or environmental factors. It does not seem likely that many people would take umbrage at the idea that the ontogenetic development of intelligence is overwhelmingly “genetically determined,” if this were paired with the claim that all variation in intelligence among persons is environmental in origin. The (mostly leftist) critics of hereditarianism clearly have been concerned with the determinants of trait/outcome variation, given that their primary moral-political goal is typically the reduction or elimination of inequality among humans, not the causal bases of trait/outcome development per se, despite their frequent (mis)use of the “genetic determinism” smear. Nevertheless, such critics are wont to observe that certain traits that are clearly under strong genetic control exhibit no variation in healthy human populations and thus would exhibit no heritability in standard behavior genetic studies (e.g., the number of chambers of the heart). This is sometimes presented as if it were a devastating critique of the usefulness of behavior genetic research in uncovering the role of genes in trait/outcome development; but since behavior genetic studies never have been intended to measure the “overall” genetic determination of traits/outcomes, but instead the relative contributions of genetic and environmental variation to trait/outcome variation, this line of attack is simply confused (see Sesardic 2005, pp. 28-33 for a more detailed treatment of this issue).

Crucially, difficulties for any effort to establish the “overall” degree of “genetic determination” of phenotypes do not apply when analyzing the causes of phenotypic variation. Since phenotypic, heritable, and environmental variation are quantifiable, statistical analyses can reveal how these variables associate in the case of any particular trait/outcome; one can establish, for example, how much phenotypic variation remains after environmental variation has been controlled statistically or via study design, and thus how much phenotypic variation may be due to variation in heritable factors (such controls will be imperfect, but will nonetheless offer insight into the relative contributions to phenotypic variation of heritable and environmental variation). (That is to say that holding other putatively causally relevant variables constant allows assessment of the potential causal effect of an uncontrolled variable on another variable; in hypothetical studies of the “overall” genetic determination of traits/outcomes, this is seemingly impossible, as genetic and environmental factors contribute to phenotypic development in all cases, and so neither class of factor can be completely controlled statistically or via study design so as to assess the isolated effect of the other.) In light of such analyses, one can determine, for example, the percentage of phenotypic variation for which heritable variation accounts. Such findings then can be evaluated alongside competing hypotheses and relevant bodies of evidence to determine which causal claims about the respective roles of heritable and environmental variation in producing phenotypic variation are best supported.

But it must be understood that what is classified as trait/outcome variation due to heritable variation in traditional behavior genetic studies does not necessarily indicate the effects of genetic variation alone. Traditional (quantitative) behavior genetic studies do not involve measurement of the effects of individual genetic variants on phenotypic variation (molecular behavior genetic studies aim to do this, however). Instead, they attempt to determine how the phenotypic similarity of individuals associates with environmental variation and genetic relatedness. For instance, a behavior genetic study may examine the phenotypic similarity of monozygotic (or “identical”) twins, who are (usually) genotypically identical, raised in distinct environments. If such genotypically identical individuals tend to exhibit high levels of phenotypic similarity across sufficiently variable environments, then there is apparent evidence that genetic factors have greater control over phenotypic variation than environmental ones. In this standard behavior genetic study design, however, anything that contributes to similarity in the phenotype under investigation of monozygotic twins raised apart should register as a “heritable” source of phenotypic variation. Conversely, any factor that contributes to dissimilarity of the phenotype under investigation of monozygotic twins raised apart should register as an “environmental” rather than a heritable source of phenotypic variation. It is known that in some cases, monozygotic twins are not in fact genotypically identical – one twin may carry mutations that the other lacks (Liu et al. 2018). Mutations are of course a potential genetic source of variation in a phenotype of interest, but if they are not common between monozygotic twins, they will not contribute to the “heritable” component of phenotypic variation in standard behavior genetic studies. By the same token, monozygotic twins raised apart may have environmental factors in common that raise their phenotypic similarity, but these would register as “heritable” sources of phenotypic variation unless they were accounted for in an appropriate way. While one should be aware of these caveats, it must be stressed that there is little reason to doubt that the heritability coefficients of traditional behavior genetic studies, which, again, indicate the percentage of phenotypic variation due to heritable variation in some population, overwhelmingly reflect the degree of genetic determination of phenotypic variation, and thus “heritable” and “genetic” are often used interchangeably in behavior genetic research. As this entry will discuss at greater length shortly, efforts to find environmental contributions to phenotypic variation that “mimic” heritable variation have not been generally successful (see, e.g., Woodley of Menie et al. 2018).

Given all of this, what can be said in favor of revised genetic determinism? The point of departure here is the substantial behavior genetics literature finding that, among individuals, variation in heritable factors (likely genes) primarily accounts for variation among adults in the four central traits/outcomes listed above. IQ, for instance, is consistently found to be 70–80% heritable by adulthood (Plomin and Deary 2015), with general intelligence, or g, having an even higher heritability of 86% (Panizzon et al. 2014; corrected for measurement reliability, Panizzon et al.’s data indicate that g is 91% heritable [Woodley of Menie, te Nijenhuis and Murphy 2014]). The factor underlying executive functions may be as much as 99% heritable (Friedman et al. 2008). Life history speed, reflected in the Super-K factor – which is superordinate to personality and (mental and physical) health, as well as various other behavioral traits/outcomes such as relationship stability, communitarian attitudes, and insight, planning, and control – is 68% heritable (Figueredo et al. 2006; note that life history speed subsumes executive functions, but the latter cluster of behavioral phenomena nevertheless has been listed as if it were a separate trait, given its unique importance in shaping human life outcomes, even among life history traits – for example, executive functions underlie the critical behavioral factor of self-control). And social status, over the course of centuries and in multiple societies, appears to be about 50–80% heritable (Clark 2014; it should be noted that in the foregoing work, Clark does not employ standard behavior genetic methods to reach his estimates, but he nonetheless provides ample evidence for the high heritability of social status; however, Clark and Cummins (2018) present further and even higher quality evidence that variation in social status is under strong genetic control).

These findings alone might appear to vindicate the revised genetic determinist view. But efforts have been made to explain such findings away, to show, in other words, that behavior genetic studies of the kind cited above have not ruled out environmental determinism (i.e., the view that environmental factors primarily or exclusively determine variation in critical human behavioral traits/outcomes). One common argument to that effect stresses that behavior genetic studies are only informative about the degree to which genetic and environmental factors explain variation in some trait/outcome within whatever population is studied. Indeed, to say that intelligence is 80% heritable is allegedly to simply assert that 80% of the variation in intelligence in a particular population is due to variation in genetic factors in that same population. Therefore, it is supposed to be difficult or even senseless to extrapolate from behavior genetic studies to broader claims about the extent to which any particular trait/outcome “in general” varies among people due to genetic variation. Further complicating the “generalizability” of behavior genetic findings is the possibility that heritability estimates at the population level are not informative about heritability at the individual level (the latter would “capture the degree to which a given trait is reliably transmitted across generations” [Woodley of Menie et al., 2015, p. 6]). Finally, and consistent with earlier discussion, critics of hereditarianism sometimes stress the fact that traditional behavior genetic studies merely report correlations between apparent sources of phenotypic variation and measured phenotypic variation. Given this, these critics are quick to observe that apparent heritable sources of phenotypic variation could in fact have no direct causal connection to phenotypic variation (see, e.g., Turkheimer 2016); to reiterate, standard behavior genetic studies do not isolate probable causal effects of individual genes, but rather estimate the degree of phenotypic variation due to variation in environmental and heritable (widely thought to be genetic) factors generally (though efforts may be made to ascertain the relative importance of additive and non-additive genetic effects and of “shared” and “non-shared” environmental effects – this entry will return to the latter topic). For example, the seemingly high heritability of IQ could reflect the mere fact that people who are highly genetically similar or even identical (identical twins) will tend to have very similar appearances. If appearance substantially influences treatment by others, and if treatment by others substantially affects IQ, then the apparent high heritability of IQ may reflect hidden gene-environment correlations (associations between genetic factors and environmental exposures) that, once properly understood, would indicate that IQ variation is under stronger environmental than genetic control.

These objections to revised genetic determinist conclusions drawn from behavior genetic research are either misleading or just incorrect, however. First, the claim that the individual-level heritabilities of traits/outcomes cannot be estimated is simply false. Woodley of Menie et al. (2015) developed a novel method by which such heritabilities can be estimated and found that, at least for the Super-K factor and related traits and factor structures, these heritabilities are broadly consistent with population-level heritability estimates in standard behavior genetic studies and are roughly the same in the USA and Sweden. Thus there is respectable evidence that population-level heritability estimates correspond to the degree to which traits/outcomes are “reliably transmitted across generations” (Woodley of Menie et al. 2015, p. 6). Second, there are good reasons to be skeptical about the insistence that the heritability of a trait/outcome “in general” cannot be derived from relevant available evidence. For it to be true that we could not make this derivation, the heritability of whatever trait(s)/outcome(s) is at issue would have to vary non-negligibly across populations or subpopulations in different environments, thereby indicating that, perhaps by way of environmental effects on gene expression, environmental factors can appreciably modify trait/outcome heritability (or at least it would have to be shown that there is no compelling evidence suggesting that environmental factors do not have this effect). But the preponderance of germane data gives no reason to believe that environmental effects are so potent, or at least no reason to believe that these effects are typically so potent. The facts that IQ is almost always found to be highly heritable by adulthood and that this has been observed in many different populations the world over suggest that intelligence exhibits developmental homeostasis, i.e., the tendency of the development of a phenotype to be largely insensitive to environmental and even some genetic variation (Sesardic 2005, pp. 75–80, makes the same essential point). Consistent with these findings, studies have generally found that variation in socioeconomic status is unrelated to the heritability of IQ, and that there are no known environmental interventions by which to reliably and lastingly raise IQ or (especially) g in healthy individuals (Protzko 2015; Woodley of Menie et al. 2018). Further to this point, variance in intelligence has not meaningfully changed over long periods of time in which enormous improvements in material quality of life and concomitant reductions in health and material wellbeing inequality (Rindermann 2018) have occurred (Rowe and Rodgers 2002). This is inconsistent with the idea that variation in IQ is to a substantial degree a result of inequality in health and material wellbeing, which environmental determinists seem to often believe.

Social status, or rather the heritable dispositions and behaviors that interact with social environments and have the effect of producing individual differences in social status, seems to be developmentally homeostatic as well. Clark’s (2014; see also Clark and Cummins 2018) research offers excellent evidence for this view, insofar as it indicates not only that the heritability of social status is roughly the same in a number of different societies with substantially different cultures and standards of living – e.g., China, Chile, Japan, Sweden, and the USA and UK – but also that the heritability of social status has hardly changed over time. In fact, the heritability of social status was, if anything, slightly lower (at times) in preindustrial England than in modern Sweden, even though the latter is widely extolled for its progressive political and economic culture. England experienced almost no change in the heritability of social status from approximately AD 1300–2000, despite “the Industrial Revolution of the late eighteenth century … the political reforms of the nineteenth century … [and] the rise of the welfare state in the twentieth century,” among many other highly significant social, cultural, technological, and economic developments (Clark 2014, p. 87). It is striking that social status, which is seemingly not biological in the way that, e.g., height is, but rather depends on complex interactions between individuals and their sociocultural environment, saw no meaningful change in its heritability over seven centuries in England during which massive and supposedly relevant environmental changes took place. Critics of behavior genetic studies, who expect that environment strongly modifies the heritability of important traits/outcomes, would predict substantial alterations in the heritability of social status from such profound environmental shifts. The relative constancy of the heritability of social status despite these changes is therefore quite devastating to the environmental determinist view. Perhaps environmental factors do more to alter the heritability of intelligence, social status, and/or other important traits/outcomes where material circumstances are much poorer than those that have been canvassed in the studies cited above. These environments must be quite rare, however, since late medieval England was extremely poor by modern standards. There is thus robust evidence that, certainly in the modern world, individual differences in important behavioral traits/outcomes are probably mostly a result of genetic rather than (nongenetic) environmental influences.

It is easy for critics of hereditarian science to posit that the heritability coefficients from standard behavior genetic studies may not track the causal effects of genetic variation on trait/outcome variation, may be contaminated with unmeasured environmental effects that mimic heritable variation, may be substantially variable across environments due to environmental effects on gene expression, and so on. Some of these possibilities are likely not favorable to environmental determinists and are probably compatible with revised genetic determinism. For example, gene-environment correlations involving environmental effects that partially produce phenotypic variation may be largely generated by genetic effects on human behavior (e.g., genetic factors leading individuals to sort into certain environments). Moreover, it is far from obvious that attempts to disrupt apparently spontaneously emerging gene-environment correlations for the sake of engendering behavioral equality would be successful (indeed, it is well known that Soviet social engineering effectively along these lines was an utter failure with morally abhorrent consequences [MacDonald 2010]).

That notwithstanding, such objections from environmental determinists are unconvincing without supporting evidence. (And, in any event, environmental determinists who are unsatisfied with hereditarian explanations that offer anything less than fully elaborated causal pathways linking genetic variation to differential behavioral traits/outcomes would do well to recognize that proposed environmental explanations of phenotypic variability are, at best, no less often and no less seriously incomplete.) Take for example the previously noted claim that the high heritability of IQ may simply reflect the tendency of people who look alike to be treated alike. As it happens, this idea has not withstood empirical scrutiny, since the correlation between physical attractiveness and IQ is near zero (Lee 2010; as Lee notes, environmental determinists could respond with the claim that some other aspect of appearance may be causally relevant – but, again, without supportive evidence, this is mere hand waving; crucially, Segal, Hernandez, Graham and Ettinger’s 2018 study of genetically unrelated “look-alikes” offers strong evidence that “[t]he criticism that [monozygotic] twins are alike in personality because their matched looks invite similar treatment by others” is false (p. 402)). This entry has already detailed the failure of efforts to find environmental effects that non-negligibly modify the heritability of IQ or social status, or to find any environmental intervention that can reliably and permanently raise IQ in healthy individuals (see also Haier 2017). Indeed, attempts to find evidence for extravagant claims about the power of environmental effects to modify behavioral trait/outcome heritability have had minimal success at best (Duncan 2014). For example, despite early findings indicating that the heritability of IQ may vary dramatically as a function of socioeconomic status (e.g. Turkheimer et al. 2003), subsequent research on this effect has determined that it is, if real at all, of very small size (see, e.g., Woodley of Menie, Pallesen and Sarraf 2018). These results align with straightforward theoretical interpretations of high heritability coefficients, i.e., that differences in traits/outcomes with such coefficients are mostly genetically determined. Moreover, it should be recognized that environmental determinists exhibit a questionable selectivity with respect to the heritability estimates about which they are skeptical. Human height is consistently found to be highly heritable, yet no one, or at least very few people, seems motivated to argue that this finding is spurious and may be due, for example, to unmeasured environmental factors that mimic heritable variation. Only in the case of politically sensitive traits/outcomes, such as intelligence, do such objections seem to be offered with any significant frequency.

General critiques of twin studies and related behavior genetic research designs abound in the academic world (e.g., Joseph 2014; Richardson 2017); but all substantive elements of these critiques have been repeatedly addressed (Barnes et al. 2014; Felson 2014; Liu et al. 2018) and have not inspired doubt regarding the soundness of these methods among the relevant scientists -- the results of twin studies are still recognized as basically accurate estimates of trait/outcome heritability and “environmentality” (see Polderman et al. 2015; see also Bouchard, Jr. 1987, 2009 on the “pseudoanalytical” nature of sweeping critiques of behavior genetics and hereditarianism). (For example, Liu et al. 2018 show that misestimation of twins’ genetic and epigenetic relatedness tends to downwardly bias heritability estimates [but only to a small extent, and primarily for high- as opposed to low-heritability phenotypes], whereas Richardson 2017 wrongly insinuates that the failure of quantitative genetic studies to accurately measure twin epigenetic relatedness generally upwardly biases heritability estimates.) Furthermore, the high heritability estimates found for a number of traits/outcomes via twin studies have been replicated using different study designs (for an example, see Schwabe, Janss and van den Berg 2017). Some argue that the “problem of missing heritability” in molecular genetic studies of complex quantitative behavioral traits – i.e. the likely causal genetic variants identified account for far less of the variation in these traits than expected in the light of traditional behavior genetic estimates – casts doubt on the validity of twin studies. However these findings are not surprising (given that molecular genetic approaches to estimating trait/outcome heritability are still in their infancy, and thus have serious limitations), and it is unlikely that phenomena that would create deep problems for standard behavior genetic estimates of trait/outcome heritability are at play, even if trait/outcome heritability is (currently) difficult to totally account for at the molecular genetic level of analysis (see Kendler et al. 2016; Kendler et al., as with Schwabe et al. 2017, offer highly compelling evidence that twin studies do not overestimate the heritability of traits, and thus that biases in twin studies likely do not contribute appreciably to the problem of missing heritability).

Though the facts thus far presented already leave the environmental determinist position very much in doubt, there are further considerations that render it clearly untenable. First, it must be recognized that environmental determinists expect or assert that environmental factors that are under human control are primarily responsible for behavioral trait/outcome variation. Intellectuals such as Kitcher (mentioned above), for example, hope that the facts about differential human behavioral traits/outcomes will be friendly to ordinary “aspirations” for, e.g., social mobility. It would hardly help their case if behavioral differences among humans were matters not of genetics but of some other biological and/or environmental factors that are outside of relevant human control (Sesardic 2005, pp. 178–182 raises the same point), such as aspects of the uterine environment or “random developmental noise” (Jensen 1980). But as it happens, understanding of whatever truly environmental effects on trait/outcome variation that behavior genetic studies may detect is quite poor – by adulthood, these influences appear to be completely independent, or nearly so, of “shared” experiences of, e.g., families and schools (shared environmental effects increase the similarity of persons living in the same household, net of the effects of genetic relatedness). They are perhaps environmental experiences that are unique to individuals, which does not inspire confidence about possible efforts to control them such as to, say, raise individuals’ IQ. And to some extent, what registers in behavior genetic studies as “non-shared” environmental effects is measurement error, and perhaps poorly understood chance events and idiosyncratic and random developmental processes. Burt, Klahr and Klump (2015) note that non-shared environmental effects are generally not stable over time prior to adulthood, which is consistent with the impression that these apparent effects are mostly “noise”; the authors do note other research showing that the effects of non-shared environment become more temporally stable in adulthood, but even then, the research that they cite suggests that only a minority of such effects are stable among adults.

The inclusion of measurement error in estimates of non-shared environmental influence probably explains the tendency for higher-precision measurements of whatever phenotype is under investigation to produce larger heritability and smaller “non-shared environmentality” coefficients. A possible example of this effect is found in Rindermann’s (2007) analysis of international differences in academic and cognitive test performance, which found that a single psychometric factor – analogous to the highly heritable g at the individual-differences level – accounted for 94–95% of the variance. This suggests the possibility that the nongenetic variance in intelligence within groups (which is typically estimated at around 20% of the variance among adults) is largely measurement error and other random factors that may be broadly the same across groups, such that genetic differences may account for almost all of the variance at higher levels of aggregation, where such evenly distributed “noise” is canceled out. The possibility that intelligence exhibits such minimal true “environmentality” is yet another piece of information that fits with the consistent failure to find any environmental variable the manipulation of which can reliably and permanently raise the IQ of healthy individuals (Protzko 2015; Woodley of Menie et al. 2018), which is to say that not only behavior genetic studies suggest the relative impotence of (controllable) environmental factors in determining variability in adult human behavioral traits/outcomes.

Additionally, Riemann and Kandler (2010) found that personality traits exhibit very high heritabilities (some around 85-90% heritable) and low “non-shared environmentalities” when multiple methods of trait/outcome measurement are used, an approach expected to reduce measurement error. By contrast, studies of the heritability of personality traits that use less sophisticated measurement techniques typically find heritabilities of 50% or less. This again indicates that a substantial portion of non-shared environmental variation found in behavior genetic studies is due to measurement error.

Studies of life history speed in humans also suggest that “controllable” environmental factors widely thought to substantially affect human behavioral variation may in fact be highly unimportant. Sociologists have long maintained that discrimination and other forms of “socially constructed” (i.e., in principle changeable through nongenetic processes) disadvantage are central to explaining correlations among mental and physical health, relationship quality, sexual behavior, subjective well-being, personality, and other domains subsumed under life history speed. Specifically, sociologists believe that discrimination on the basis of and other disadvantages associated with differences of race, sex, and class explain a great deal of human behavioral variation. But it turns out that the latter sociological variables, even when all pooled together (and with educational attainment added), explain at best less than 10% of the variance among life history traits, whereas the highly heritable Super-K factor explains nearly all (91%) of the variance (Figueredo et al. 2007). The failure of these variables, which are so central to mainstream sociological theory and analysis, to meaningfully explain the interrelations of such critical human traits/outcomes is remarkable.

Finally, it must be noted that to the extent that environment matters for important human behavioral traits/outcomes, some of the relevant environmental factors are likely genetic. There is a substantial literature on social epistasis, i.e., inter-organismal genomic transactions whereby the genotype of one organism affects the gene expression and phenotypic development of another organism (see Woodley of Menie et al. 2017b). Revised genetic determinism therefore extends in a surprising way to the environment as well.

Furthermore, though much has been made in some quarters about the power of environmental factors to epigenetically modify organisms, those offering such claims frequently miss the fact that epigenetic effects operate by way of preexisting genetic potentials and do not undo the significance of (likely) genetic variation captured in standard heritability coefficients (Figueredo et al. in preparation).

Critics of hereditarian science should recognize that attempts to trivialize the role of genes in determining individual differences easily fall into opposition to basic principles of modern evolutionary theory. Evolution via selection simply is differential reproductive success as a function of heritable phenotypic variation and environmental circumstances (with heritable factors subject to mutation). If traits cannot be reliably transmitted across generations, because they are open to such radical environmental/epigenetic alteration that genetic variation should not be expected to yield at least fairly reliable patterns of trait/outcome variation, then it would seem that the very idea of evolution by selection is in trouble. This implication suggests that the efforts of anti-hereditarians to attenuate or even sever the connection between inter-individual genetic and trait/outcome variation are without much sense.