As cancer cells often display transcriptional addiction to support their rapid growth and survival, it is worth noting that treatment with roniciclib induced rapid Ser-2 dephosphorylation in the C-terminal domain of RNA polymerase II (Fig. 3c), a target of CDK9/cyclin T. Further, roniciclib also suppressed the phosphorylation of retinoblastoma protein (pRb; Figs. 2a and 3c), which implies reduced bioavailability of the transcription factor E2F1.17,18 We also examined MCL-1, an anti-apoptotic protein transcribed by RNA polymerase II. The gene discussed is CDK9; the disease is cancer.