Since DAPK1 is known to phosphorylate Ser71 of Pin1 and inhibits the prolyl isomerase activity [57], we speculate that the DAPK1-induced APP phosphorylation and the cis pThr668-Pro APP accumulation caused by DAPK1-induced Pin1 suppression both contribute to the excessive generation of Aβ in AD. This evidence concerns the gene PIN1 and Alzheimer disease.