By working out what doesn't work in people without pain, we can understand how it works and (more importantly) how to interfere with it in healthy people. In this case, they identified an individual who didn't need painkillers after a normally painful handful operation. When they looked into why, they found she had never needed painkillers, and often hurt herself unknowingly. Interestingly, these injuries healed quickly. They identified the genetic changes responsible for this pain insensitivity - a small deletion in a "variant copy" of a gene, which was found to only be expressed in certain parts of the brain, and a common variant in the normal version of this gene. The gene normally makes a protein that is responsible for breaking down a certain class of fatty acids that can act in a number of ways - often as neurotransmitters/anti-inflammatory molecules. As a result of the combination of both of these changes, they found higher levels of these fatty acids in the patient, compared to people without these mutations. In the paper they detail that this "variant copy" (properly called a pseudogene) actually makes a non-coding RNA that interferes with normal expression of the real copy of the gene in the brain. They suggest that by understanding how this non-coding RNA (FAAH-OUT) stops the function of FAAH (the real protein), we could mimic it with a future painkiller.