Whereas for AD there is abundance of evidence pointing to a pathogenetic role of SET associated to its inhibitory effect on PP2A and on the downstream hyperphosphorylation of tau, it is not completely understood whether PP2A inhibition could explain the plethora of oncogenic effects mediated by SET or if other SET functions, including inhibition of acetyltransferase or binding to specific partners, contribute to cancer progression and development of drug resistance. This evidence concerns the gene SET and Alzheimer disease.