Additionally, Src inhibitors oppose activating phosphorylation of the STAT3 transcription factor, which inhibits the transcription of multiple genes that encode protein implicated in AML survival and proliferation e.g., MCL-1,18 BCL-xL,52 and c-MYC.55 Furthermore, combining MCL-1 with Src inhibitors leads to pronounced up-regulation of NOXA, a well-established promoter of MCL-1 degradation.34 Collectively, these pharmacodynamic events trigger a marked potentiation of BAX/BAK-mediated cell death and synergistic anti-AML activity. The gene discussed is SRC; the disease is acute myeloid leukemia.