These effects are exerted by multiple, complimentary mechanisms involving modulation of FLT3 protein levels, inactivation of the MAPK/ERK and JAK2/STAT5 pathways, reduction of Mcl-1 and c-Myc, induction of Bim, and downregulation of cellular metabolites, leading to synergistic antileukemic activity against FLT3-ITD AML. The gene discussed is MCL1; the disease is acute myeloid leukemia.