While therapeutic agents targeting AD pathologies, β-amyloid (Aβ) plaques and tau neurofibrillary tangles (NFTs), are in development and anti-Aβ monoclonal antibodies have been given FDA approval (e.g., aducanumab [2], lecanemab, and donanemab) [84], there is still need to develop disease-modifying therapeutics targeting other pathologic mechanisms of AD to be used separately or in combination. The gene discussed is MAPT; the disease is Alzheimer disease.