In AD, it not only enhances the β-site amyloid precursor protein cleaving enzyme 1 (BACE1)-mediated cleavage of amyloid precursor protein (APP) to generate aggregation-prone Aβ1–42 and promote Aβ aggregation, but also activates stress kinases, particularly the p-JNK pathway, to drive tau hyperphosphorylation. This evidence concerns the gene APP and Alzheimer disease.