Just when you thought you understood genetics, researchers have shown up with a new term that sounds sort of like the old term but isn’t. Meet epigenetics—the non-DNA way things are inherited.

Though the distinction may seem arcane (see below for definitions), understanding epigenetics is crucial to follow developments across all of medicine, including the latest in cancer research. Last week, for example, an interesting scientific article appeared that examined the epigenetics, not genetics, of kidney cancer cells and suggested a path forward to possible new treatments. And this is one of many similar articles in the field that focus on the epigenetic drivers of tumors.

What, then, is epigenetics and why do you need to know about it? We are all familiar with the super-simple, super-clear Watson and Crick world of the double helix. Here, spinning and zipping seemed to explain how Johnny got red hair from his grandmother and that funny-looking chin last seen on an uncle whom no one likes.

But as with all things in science, that which appears simple always is vastly more complicated. The great simplifying insights, such as that of Watson and Crick, provide the critical scaffolding for progress, but never are the final explanation.

Though science class may be a nightmare from which you were unable to awaken, you may remember that DNA is composed of a very small alphabet: there are four different possible chemical structures—adenine (A), cytosine (C), guanine (G), and thymine (T). Together this troupe spells out all of the genetic information across the entire 20,000-25,000 human genome, in jammed typewriter fashion: AACTGTTTCATC, ad infinitum. Truly infinitum.

But wait, there’s more. As with all endeavors, in addition to the front lines of ACTG, there is middle management, aka epigenetics. It turns out that the simple zipping and unzipping—that dance of replication—needs more organization, more oversight, more focus on what is mission critical.

This then is the task of epigenetics: It refers to a set of other chemical structures that tell the zipping ACTG when to start and when to stop, when to bend and when to twist, when to reap and when to sow. Without this next level of organization, the well-meaning but somewhat blind activity of DNA replication would create lengths of beautiful but unusable ATCG gobbledy gook.

Most experts trot out the story of bumble bees to further explain epigenetics. A few years ago, researchers at Johns Hopkins examined a bumble bee paradox: A beehive is composed of a queen bee, some male drones, and some sterile female worker bees. Among the worker bees, some nurse and some forage, completely different activities. The paradox is this—the foragers and the nursers have an identical genetic makeup.

The explanation of this non-genetic differentiation is that the bees’ epigenetic profile promotes the forage-nurse differentiation by chemically tagging certain parts of the down-stream DNA products. Presto—a perfectly functioning beehive that hums, well, like a beehive. Leave it to middle management to take all the credit.

The promise of epigenetics, and not just genetics, is this: Science has moved very quickly in the last decade by exploiting insights into the ACGT of cancer. In other words, where a single gene mutation is at the heart of a problem, researchers can now sculpt a medicine to address the hiccup in pretty short order.

The problem is that single gene problems don’t explain a large swathe of human disease. For this group, there is hope that medical manipulation of epigenetic starts and stops—and not genetic starts and stops—will provide a second generation of fresh insights and methods to get at the cancer where it really lives, at the molecular level. And what better place to start than in persons with advanced cancer, where the cell long ago has moved past simple single gene mutations.

For those who want more, I refer you to the kidney cancer article in the very prestigious journal, Oncogene. One note of caution—here is their kicker sentence: “These data suggest that during progression of ccRCC [some types of kidney cancer], a decline in H3K36me3 is observed in distant metastases, and regional H3K36me3 alterations influence alternative splicing in ccRCC.”

In other words, though extremely exciting, the impact this year of our growing insights into epigenetics on treatment of a person with cancer or other diseases will be nil. Probably not next year or the year after either. But this is how real science moves forward—smart researchers who puzzle over cells and enzymes, who ignore the conventional wisdom even on something as etched-in-stone as the gene, and who speak a language sealed off from the rest of us (“H3K36me3 alterations,” anyone?). So even though the attention given this particular article and approach is overblown, the implicit endorsement of cold, hard science, and of cold, hard scientists, surely is not.