The classical Aβ hypothesis of AD claims that the mutant or misexpression of APP generates excessive Aβ (Hardy and Selkoe, 2002), leading to neurotoxicity (O'Brien and Wong, 2011), neuroinflammation (Cai et al., 2014), and regeneration deficiency (Scopa et al., 2019). The gene discussed is APP; the disease is Alzheimer disease.