Furthermore, EPI reduces the sensitivity to apoptotic cell death mechanism in prostate and breast cancer cells through interaction with β-ARs and in turn the β-ARs/cAMP/PKA signaling pathway promotes the phosphorylation and consequent inactivation of pro-apoptotic protein BCL2-associated death promoter (BAD) [17] confirming that signaling through β-adrenergic receptor can enhance tumor survival through multiple intracellular pathways. Here, CTBP1 is linked to neoplasm.