A subgroup analysis of the VIALE-A trial showed inferior OS for patients with FLT3-ITD mutated AML receiving HMA plus venetoclax compared to FLT3 wild-type AML (median OS 9.9 vs. 14.7 months, respectively) [62]: FLT3-ITD mutations promote venetoclax resistance via BCL-2 and MCL-1 overexpression [63]. Here, FLT3 is linked to acute myeloid leukemia.