ABL1 and acute myeloid leukemia: Although such inhibitors may not be as specific as those directly targeting oncoproteins that drive transformation (e.g., BCR/ABL in CML, FLT3 mutations in AML, and EGFR mutation or EML4-ALK fusion protein in NSCLC), they may disrupt the mechanisms required for maintaining survival of transformed cells and thus play an important adjunctive role in various DTT approaches.