Although the pathogenesis of AD is complex and has not been completely elucidated, investigation of disease neuropathology has led to considerable evidence supporting “Aβ hypothesis.” It posits that Aβ upregulation and accumulation are the primary pathological events of AD, which induce phosphorylated Tau (pTau) in neurons, followed by neurofibrillary tangle formation and neuroinflammation, as well as synaptic dysfunction and loss, and ultimately, neurodegeneration (4, 5, 6, 7). The gene discussed is MAPT; the disease is Alzheimer disease.