Findings need to be validated in larger numbers of patients with AME associated with autoantibodies against NMDAR, LGI1, and other antigens, acknowledging the broad variability in the clinical phenotype and long-term outcomes in AME (1–6, 9) and the low likelihood of detecting rare events (i.e., motor vehicle accidents) in small cohorts of patients. The gene discussed is LGI1; the disease is apparent mineralocorticoid excess.