With regard to APP, elegant study performed by Anandatheerthavarada and his colleagues [30] revealed that C-terminal truncated APP (lacking Aβ) targets mitochondria in cholinergic, GABAergic, dopaminergic, and glutamatergic neurons of AD brain by clogging up mitochondrial protein translocase complex TOM40/TIM22. This evidence concerns the gene APP and Alzheimer disease.