CDK9 is permissive for transcription by phosphorylation of RNA polymerase II on serine 2 (RPIIS2), and in AML cells TG02 treatment causes rapid RPIIS2 dephosphorylation, such that RNA synthesis is strongly inhibited [16–18] and proteins with a short half-life, such as MCL-1, are rapidly downregulated [16, 17]. Here, MCL1 is linked to acute myeloid leukemia.