Consistent with the implications of our study, Fidelman [58] et al. suggested that AEA was decreased in CA1 of the hippocampus after shock, and that improving endocannabinoid signaling through the application of a fatty acid amide hydrolase (FAAH) inhibitor, URB597, has the potential to alleviate PTSD-like behaviors in rodents. The gene discussed is FAAH; the disease is post-traumatic stress disorder.