In addition to the Aβ hypothesis, tau hypothesis, and neuroinflammation hypothesis, recent years have seen the proposal of viral, mitochondrial dysfunction, insulin signaling abnormalities, gut microbiota dysbiosis, excitatory amino acid toxicity, and cholinergic dysfunction hypotheses, further enriching the research on the pathogenesis of AD (6, 18–22). The gene discussed is MAPT; the disease is Alzheimer disease.