However, the knowledge that CDKI-73 is ~6–80-fold more active against CKD9 than these other CDKs in vitro [56] and the pharmacodynamic readouts evaluated in this study (i.e. inhibition of RNAPII pSer2 and AR pSer81 phosphorylation, reduced levels of MYC and anti-apoptotic proteins, impingement of BRD4 activity and an overall reduction in transcription) collectively support the concept that inhibition of CDK9 is the major mechanism by which CDKI-73 exerts anti-tumor activity in prostate cancer. This evidence concerns the gene CDK9 and neoplasm.