Woods was aware that the Wolfson Institute, John Wood’s lab, had recently published a paper on an inherited phenotype—essentially a collection of observable characteristics, such as eye color—that appeared to influence pain resistance. Perhaps, Woods theorized, the boy in Pakistan possessed the same phenotype. When Woods found the boy’s family, they told him that the boy had died from injuries sustained during a stunt leap from a rooftop. But several family members allowed Woods to collect blood samples, which researchers in England, using what was then cutting-edge software, scanned for genetic irregularities.

Sure enough, the Pakistani subjects all possessed the same abnormality Wood’s lab had documented: a subtle mutation in a gene regulating pain-sensing neurons, which disabled a key component known as Nav1.7. In a typical healthy adult, Nav1.7 helps notify the brain of pain or discomfort. When it’s removed or defective, no pain signal can be sent.

In 2006, with Woods as lead author, the scientists published their findings in the journal Nature. The reception was ecstatic. The work, one British reporter marveled at the time, “could lead to a safer range of pain-killing drugs.” Soon, several pharmaceutical companies unveiled plans to develop a drug to “block” Nav1.7. (Those efforts, though ongoing, have not yet panned out—scientists have had trouble getting the drug to cross the blood-brain barrier, where Nav1.7 does much of its work, among other challenges.)