While such TKIs have primarily been used in the setting of BCR/ABL+ leukemias,46 Src promotes AML cells survival, and Src inhibitors have demonstrated anti-AML activity in pre-clinical studies.24 While the possibility that the TKI-related inhibitory activity of these agents contributed to the prevention of MCL-1 accumulation cannot be ruled out, the finding that Src knock-down recapitulated the effects of pharmacologic agents (e.g., MCL-1 down-regulation and increased apoptosis) argues strongly that Src disruption plays a significant functional role in these events. The gene discussed is SRC; the disease is acute myeloid leukemia.