We previously demonstrated that lentiviral Aβ1-42 expression leads to p-Tau accumulation and inhibition of both the proteasome and autophagy [13, 14, 16, 17], while the Abl tyrosine kinase inhibitor Nilotinib increases autophagic Aβ and p-Tau clearance, leading to decreased plaque levels in AD models [14, 16]. This evidence concerns the gene MAPT and Alzheimer disease.