To confirm that the system developed in this study is able to recapitulate the various AD-associated phenotypes, including extracellular Aβ accumulation and Tau protein phosphorylation, we compared the iNs derived from AD patients with APP or PSEN1 mutations or with the ApoE ε4 polymorphism to those from normal subjects (Table 1). The gene discussed is PSEN1; the disease is Alzheimer disease.