Consistent with these central functions, MEF2C has been found to be aberrantly expressed in subsets of T cell acute lymphoblastic leukemia (T-ALL) and in early thymocyte precursor (ETP) T-ALL in particular, an aggressive leukemia that tends to be refractory to chemotherapy and shares genetic features with AML [7–10]. Here, MEF2C is linked to acute myeloid leukemia.