In both hematologic malignancies and solid tumors, there is increasing evidence that CDK9 activity is required to maintain sufficient levels of short half-life transcripts and proteins such as mixed-lineage leukemia (MLL)-fusion genes products, the antiapoptotic myeloid cell leukaemia-1 (MCL1) protein, and the proto-oncogenes MYB and MYC, which cancer cells are dependent upon for their survival (13–16). The gene discussed is KMT2A; the disease is cancer.