Recent reports foster yet another theory: AD is a disease triggered by impaired APPs to establish a link between the loss metabolism, further promoted through tau pathology instead of Aβ amyloids; in short, very recently, a critical role for amyloid precursor protein (APP) and presenilin (PS) mutations in familial AD was highlighted, underlining that the trigger of AD might rather be linked to impairments of APP metabolism and an accumulation of APP C-terminal fragments. The gene discussed is APP; the disease is Alzheimer disease.