But perhaps the most common hypothesis is that big animals simply have more anti-cancer defenses, including the “tumor suppressor” genes that stop cancers from developing. That idea was on Vincent Lynch’s mind in 2012, when he agreed to give a guest lecture on Peto’s paradox. “I was sitting at my computer, and I thought: Let me just look at the elephant genome and see if they have extra tumor suppressors,” says Lynch, who is an evolutionary biologist at the University of Chicago. “It turns out they have lots. And then I had something to tell the class.”

At first, Lynch looked at specific tumor-suppressor genes like p53. Nicknamed the “guardian of the genome,” p53 plays a pivotal role in responding to damaged DNA, which could ultimately lead to cancer-causing mutations. When such damage is detected, p53 activates other genes that try to fix the problems. It stops cells from growing while those repairs are underway. And if the damage is irreparable, it triggers a self-destruct system that forces the affected cells to commit suicide, before they can turn into tumors.

We have one copy of p53. Lynch discovered that elephants have 20. (A second team independently made the same discovery at the same time.) These extra copies make elephant cells exquisitely sensitive to damaged DNA, and they’ll launch their self-destruct programs at levels of damage that human cells would tolerate. This hair-trigger propensity for cellular suicide helps to explain why elephants are so resistant to cancer for an animal of their size.

But p53 is only part of the story. Lynch’s student Juan Manuel Vazquez found that elephants also have many extra copies of another tumor-suppressor called LIF, as do their closest relatives—the large aquatic manatees, and the tiny rodent-like hyraxes. Millions of years ago, in the common ancestor of all these species, the original LIF gene was accidentally duplicated many times over, creating the extra copies that exist today.

Most of these copies are “pseudogenes”—dead or dormant genes that don’t actually do anything. That’s because the same duplication events that created them failed to copy their promoters—small stretches of DNA that sit in front of genes and allow them to be switched on. Creating a gene without a promoter is like building a car without an ignition switch. You have something that could work, but doesn’t.

There’s one exception. Vazquez found that one of the elephant’s nine extra LIF genes—LIF6—does work. When LIF6 was first created, by fortunate happenstance, the random stretch of DNA just ahead of it was already pretty close to being a promoter. It only took a few small changes, acquired over the course of elephant evolution, for that sequence to evolve into a brand new promoter, allowing the once-dormant LIF6 to whirr into life.

Now, when DNA gets damaged, p53 lands at the promoter and spurs LIF6 into action. LIF6 then triggers that self-destruct sequence that sends damaged cells to their doom. For good reason, Lynch calls it a zombie gene—it used to be dead, it’s now reanimated, and it kills the cells that rouse it.