A great effort was spent on restoring PP2A activity in pancreatic cancer and AML by means of genetic approaches aiming to knock down the PP2A endogenous inhibitors, SET and CIP2A, as well as pharmacological approaches using PP2A activating drugs (PADs) or small-molecule activators of PP2A (SMAPs) to prevent tumor growth and overcome therapy resistance [5,10,168]. This evidence concerns the gene PTPA and acute myeloid leukemia.