In contrast to the APPPS1 mouse model that overexpresses mutated human amyloid precursor protein (APP) and presenilin-1 (PS1), the APP-KI model bears endogenous levels of APP with a humanized Aβ sequence containing three AD mutations (NL-G-F), and has no alterations of PS1 (Radde et al., 2006; Saito et al., 2014). The gene discussed is APP; the disease is Alzheimer disease.