While patients with FLT3 or IDH1/2 mutated AML have encouraging outcomes with VEN combinations, treatments targeting other molecular subgroups (i.e., TP53, N/KRAS mutated) and inhibitor combinations (i.e., MCL1 inhibitors which have demonstrable cardiac toxicity) require further optimization and study. The gene discussed is FLT3; the disease is acute myeloid leukemia.