By binding to the bromodomains of BET proteins (BRD2, BRD3, BRD4, and BRDT), these inhibitors obstruct the recognition of acetylated histones, leading to the suppression of key oncogenes such as MYC, BCL2, and TMPRSS2-ERG, which are essential for tumor proliferation, survival, and resistance to therapy [205]. Here, BRD4 is linked to neoplasm.