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. This evidence concerns the gene ALK and chronic myelogenous leukemia, BCR-ABL1 positive.