Specifically, there are three described mechanisms by which SET has been shown to become an active PP2A inhibitor: (i) overexpression of SET is detected in several leukemias, Wilms tumors (9, 29), epithelial ovarian cancer (35), prostate cancer (36), and lung cancer (12); (ii) altered phosphorylation of SET was observed in prostate cancer, PV, Alzheimer’s disease, and in activated T-cells with the suspected kinases defined as PKC, casein kinase II, and PKD, respectively. This evidence concerns the gene PRRT2 and prostate carcinoma.