Clark stumbled upon the PON1 story by accident, while trying to understand what happens when mammals adapt to a life at sea. Many groups have independently made that transition: Hoofed relatives of deer and hippos gave rise to whales and dolphins; bulky cousins of elephants gave rise to manatees; and meat-eating relations of bears gave rise to seals and sea lions. These changes all happened independently, but the sea-going species all evolved streamlined bodies and flipper-like limbs. And as their physiques converged, so did their genes. Every time mammals adapted to the oceans, hundreds of genes began evolving at a quicker pace, and others at a slower one. And some genes were repeatedly broken.

Clark’s colleague Wynn Meyer scanned the genomes of 58 mammals in search of genes that look much the same in land-living species, but have repeatedly accumulated disabling mutations in the marine lineages. She found several, most of which are involved in smell—the sense that marine mammals lack. But sitting at the very top of the list was a gene with no connection to smell at all—PON1. “We definitely weren’t expecting that,” Meyer says.

PON1 acts as an antioxidant. It breaks down fatty acids that have reacted with oxygen molecules, and that lead to inflammation and heart disease if they’re allowed to build up. It’s clearly important—so why should mammals lose it every time they evolve for a seagoing existence?

The team doesn’t know, but they have a guess, and it involves the deep breaths of diving mammals. “They’re packing their bodies full of oxygen and going underwater for up to an hour,” Clark says. “They then completely deplete that oxygen before going back up and reperfusing themselves.” Whales can tolerate those fluctuations, but humans can’t. Even if we didn’t suffocate, we’d flood our bodies with unstable oxygen molecules that would royally mess up our cells.

Diving whales and seals adapted to this challenge by mass-producing enzymes that mop up the oxygen molecules before they do much damage. And perhaps, after the conscription of these new biochemical guardians, “PON1 got left by the wayside,” Meyer says. “Maybe other proteins took on the job that PON1 used to do.” When the gene started to deteriorate, its oceangoing owners didn’t notice, because they had other antioxidants at play. “It makes sense from an evolutionary perspective,” says José Pablo Vázquez-Medina from UC Berkeley, who was not involved in the study.

Whatever the reason, the result is clear. As far as we know, every mammal that lives on land has a working copy of PON1. But whales, manatees, and seals all independently broke their versions of the gene between 21 and 64 million years ago. Even partially aquatic mammals, like the beaver and sea otter, have lost PON1. And in the modern era of organophosphates, that loss could take a newfound toll.