Previous observations show that: 1) in nonobese, but not in obese, individuals, insulin negatively controls AEA more significantly than 2-AG blood levels [8], possibly by stimulating the expression of FAAH [6], which is more specific for AEA than 2-AG; and 2) circulating leptin levels are negatively associated with blood AEA, but not 2-AG, levels in lean, but not in obese, women with eating disorders [35], although leptin reduces both AEA and 2-AG levels in mouse adipocytes [3]. The gene discussed is FAAH; the disease is eating disorder.