Recently, several preclinical studies reported that the pharmacological restoration of PP2A tumor-suppressor activity by PADs effectively antagonizes leukemogenesis, and the anticancer activity of PADs usually depends on interactions with PP2A’s endogenous inhibitor, SET, an oncogene overexpressed in 28% of AML patients [9, 44, 45]. The gene discussed is SET; the disease is acute myeloid leukemia.