FAAH2 is an X-linked enzyme that catalyzes hydrolysis of endogenous fatty amides, including the endocannabinoid anandamide and sleep-inducing oleamide, to their corresponding fatty acids 12. The enzyme preferentially hydrolyzes monounsaturated substrates and contains a critical amidase signature domain required for catalytic activity 3. FAAH2 is expressed in multiple tissues, including seminal vesicles where it localizes to epithelial cells, skeletal muscle, and adipose tissue, regulating endocannabinoid signaling and stress responses 456. Loss-of-function mutations in FAAH2 are associated with neuropsychiatric and metabolic phenotypes. A hemizygous variant (p.Gln330Lys) presented with anxiety disorder, autistic-like traits, borderline intellectual functioning, obesity, and hepatic steatosis 3, while a maternally-inherited missense mutation (p.Ala458Ser) caused autism with subsequent anxiety, ataxia, and learning disabilities accompanied by lipid metabolism abnormalities 7. Clinical exome sequencing identified FAAH2 as a candidate disease gene 8, and molecular autopsy studies support its role in lethal conditions 9. FAAH2 dysregulation has been implicated in late-onset preeclampsia pathophysiology 10. These findings suggest FAAH2 variants contribute to X-linked neurodevelopmental disorders with metabolic involvement through altered endocannabinoid signaling.