Despite the confirmation of pathological features such as extracellular β-amyloid (Aβ) plaques, excessive tau phosphorylation, and abnormal neurofibrillary tangles (NFTs) from the biochemical anatomical results of brain tissue in AD patients, the detailed mechanism of AD is still not completely understood, and effective disease-modifying treatments are largely limited and lacking (Qiang et al., 2017; Fortea et al., 2020). The gene discussed is MAPT; the disease is Alzheimer disease.