We and other groups have shown that deregulation of some PP2A subunits, deregulated expression of the endogenous PP2A inhibitors SET or cancerous inhibitor of protein phosphatase 2A (CIP2A), or overexpression of SETBP1, contribute to PP2A inhibition in AML (28, 30, 40, 49, 50). The gene discussed is CIP2A; the disease is acute myeloid leukemia.