In this respect, protein kinase C (PKC) agonists have a substantial record of cytostatic and cytotoxic effects in multiple cancer models, often linked mechanistically to overactivation of the MAPK pathways [21, 22, 23] However, sustained activation of PKC isozymes leads to the downregulation of their protein levels [24], imposing a potential handicap for the therapeutic use of these molecules. This evidence concerns the gene PRRT2 and cancer.