While treatments with combinations of the STAT5 inhibitor AC-4-130 with the FLT3 inhibitor midostaurin (PKC412), the BMI1 inhibitor PTC596 or the MEK inhibitor trametinib were rather ineffective, the combination of AC-4-130 and the MCL1 inhibitor S63845 led to a significant reduction in cell viability in a larger subset of AML. The gene discussed is STAT5A; the disease is acute myeloid leukemia.