Since the amyloid hypothesis proposed by Hardy and Allsop et al. (1991), Aβ has been thought to be the main causative factor for AD [17], who identified a mutation in the amyloid precursor protein (APP) gene on chromosome 21, and suggested that APP mis-metabolism and Aβ deposition were key drivers in the pathological cascade of AD [17,18]. The gene discussed is APP; the disease is Alzheimer disease.