Given that the MAPK pathway is activated in about 70% of patients with AML due to mutations in upstream key proteins including RAS and FLT3 (33), and recent studies which show that further mutations in MAPK can arise from use of venetoclax or targeted therapies like gilteritinib (FLT3i), the use of a MEK inhibitor like selumetinib as a combination partner has strong rationale (34). The gene discussed is FLT3; the disease is acute myeloid leukemia.