The observation that drugs targeting the RAAS, whether ACEIs, ARBs, or AT2R agonists, preserve memory and attenuate amyloid- and tau-related pathology in animal models, coupled with epidemiological and clinical findings linking RAASi use to a lower incidence and slower progression of AD in humans, provides further evidence that dysregulated angiotensin signaling actively contributes to AD (73, 108, 132–136). The gene discussed is MAPT; the disease is Alzheimer disease.