As expected, the suppression of CDK9 activity and expression by dinaciclib caused decreases of anti-apoptotic proteins c-FLIP, Mcl-1 and Bcl-2 expression and increase of pro-apoptotic protein Bax expression in this study, subsequently resulting in strikingly promoted apoptosis induction by EV-T in cancer cells. The gene discussed is CFLAR; the disease is cancer.