CDK9, a key protein in the positive transcription elongation factor complex b, is a known regulator of transiently expressed prosurvival genes, including but not limited to Mcl-1, Cyclin D1, and c-Myc.19,20 Inhibition of CDK9 with flavopiridol (alvocidib; in phase 2 clinical trials in AML and tolerated in elderly patients) can downregulate Mcl-1 and cooperate with venetoclax in AML.21–23 There, however, remain concerns about the off-target toxicity of flavopiridol. The gene discussed is CDK9; the disease is acute myeloid leukemia.