The CRISPR-edited babies might have shortened lifespans.

Why? Well, as Nature explains, we’ve just found out that the same gene combination that gives HIV resistance to those kids He Jianku worked on also makes them 21% likelier to die before their 76th birthday:

The analysis is based on genetic and health data from nearly 410,000 people enrolled in the UK Biobank research project. The study’s authors did not have enough data to estimate survival probabilities beyond the 76-year mark.

CCR5 encodes a protein that allows HIV to enter immune cells. Deleting part of the gene can disable it — mimicking a naturally occurring mutation, CCR5-Δ32, that confers resistance to HIV. Researchers were also concerned about evidence suggesting that the CCR5-Δ32 mutation makes people more susceptible to the effects of infection by influenza and West Nile virus.

Around the time of He’s announcement, evolutionary biologist April Wei of the University of California, Berkeley, was developing a computational tool to link genetic mutations with lifespan, using data from the UK Biobank. She and geneticist Rasmus Nielsen, also at Berkeley, decided to test the tool with CCR5. “It’s an interesting gene on its own,” Wei says.

All mammal genomes contain a version of CCR5, suggesting that it has an important role in these animals΄ biology. Yet the CCR5-Δ32 mutation is common in some human populations. About 11% of the UK population carries the mutation in both copies of the CCR5 gene, and the rate is even higher in parts of Scandinavia.

Mutations that delete part of a functional gene are rarely so widespread. The prevalence of CCR5-Δ32 suggests that, at least in some cases, disabling the CCR5 gene can confer an evolutionary advantage, Murphy says. But scientists don’t know what that might be.