Even though the patient's microdeletion is in the pseudogene of FAAH, not the gene itself, the pain genetics teams wondered if the mutation was somehow affecting her anandamide levels. And, indeed, it was. Her circulating levels of anandamide were 70 percent higher than is typical. The researchers aren't sure exactly how the pseudogene plays a role here, but intend to pursue that question further. Perhaps FAAH-OUT could be a useful drug target, especially given how unsuccessful it’s been to target FAAH directly.