Overall, we identify genomic alterations that correlate with midsotaurin response independent of FLT3-ITD status, propose that Ras-Raf-MEK-ERK inhibition in combination therapy could limit resistance to midostaurin, and suggest that within the overall AML population there may be therapeutic benefit of midostaurin in patients with certain expression profiles. The gene discussed is MAP2K7; the disease is acute myeloid leukemia.