PP2A: Inactivation through phosphorylation is seen in primary AML cells for a majority of patients; this inactivation can be caused by either deregulated expression of endogenous PP2A inhibitors (e.g., SET, see above), overexpression of SETBP1 or downregulation of PP2A subunits [134]. This evidence concerns the gene SETBP1 and acute myeloid leukemia.