Amongst these models, the 5xFAD (familial Alzheimer’s disease) mice rapidly generate high levels of the most pathogenic and aggregate-prone Aβ1–42 form, driven by the presence of 3 mutations in the human knock-in amyloid precursor protein (APP) and 2 mutations in the human presenilin-1 (PSEN1) genes that are linked with AD [18]. The gene discussed is APP; the disease is Alzheimer disease.