But one thing didn’t work at all the way the scientists expected. Of the 42 successfully corrected embryos, only one of them used the supplied template to make a normal strand of DNA. When Crispr cut out the paternal copy—the mutant one—it left behind a gap, ready to be rebuilt by the cell’s repair machinery. But instead of grabbing the normal template DNA that had been injected with the sperm and Crispr protein, 41 embryos borrowed the normal maternal copy of MYBPC3 to rebuild its gene.

Which is why Mitalipov insisted on the title given to their paper: “Correction of a Pathogenic Gene Mutation in Human Embryos.” “Everyone always talks about gene editing. I don’t like the word editing. We didn’t edit or modify anything,” Mitalipov says. “All we did was unmodify a mutant gene using the existing wild type maternal gene.”

The next step will be to see if they can replicate this “unmodifying” effect in different mutations. The MYBPC3 gene had four messed up base pairs, so it was pretty easy for Crispr-Cas9 to find and replace. But other mutations might be off by just a single letter, which would be harder to fix. There’s always a chance that MYBPC3 will have been a case of beginner’s luck, so they want to make sure the effects are generalizable to other common mutations, like the BRCA genes associated with increased risk for breast and ovarian cancers.

Crispr experts around the globe were quick to celebrate the work while pointing out its many limitations. “This is a remarkable paper that shows how much the field has progressed in just the last year or two,” says Gaetan Burgio, a geneticist at the Australian National University. “But I think for now everyone needs to chill down a bit. The scope is very limited, and it’s unlikely to me that Crispr would be a substitute for preimplantation genetic diagnosis, whatever the authors say.” Burgio is referring to the genetic profiling of embryos prior to implantation via IVF—it’s a way to screen for mutated genes like MYBPC3 and only select the 50 percent of embryos that are normal.

Mitalipov and his coauthors argue that their Crispr technique can get that number up to around 75 percent, maybe even 100. Which would prevent prospective moms, especially older ones, from having to go through multiple rounds of costly, unpleasant egg harvesting.

But validating that kind of treatment would require lengthy clinical trials—something a rider in the current Congressional Appropriations Act has explicitly forbidden the Food and Drug Administration from even considering. Mitalipov said he’d have no problem going elsewhere to run the tests, as he did previously with his three-person IVF work. Before that, he’d need to re-run these experiments in animals, and implant the embryos to assess them at different developmental stages for any abnormalities. Collaborators like Jun Wu at the Salk Institute will likely follow up in another way, with more stem cell studies, to see if the Crispr corrections follow cells through all their different lineages—into neurons and liver cells and heart cells.

If there’s anything Wu and Mitalipov and the rest of their team have learned through all this, though, it’s that stem cells and embryos are not re-created equal. Because the early days of embryonic development are so tumultuous, with lots of dividing and recombining, those cells might have special ways to avoid genetic mishaps—like, say, copying a random piece of DNA that a scientist stuck into a cell. Evolution may have made it harder than anyone thought to subvert its will with superbaby genes.