Histone acetyltransferase E1A-binding protein p3 (EP3), tumor protein p53 (TP53) and B-cell lymphoma-2-associated X protein (BAX) contribute to the regulation of the cell cycle and apoptosis, cellular processes that are often impaired in cancer cells. The CREB (cAMP responsive element binding protein) binding protein (CBP) and its homolog EP3 have emerged as new therapeutic targets for the treatment of cancer and inflammatory diseases. CBP/EP3 inhibitor 29h represents a promising lead compound for the development of new therapeutics for the treatment of castration-resistant prostate cancer. the bromodomains of the histone acetyltransferases CREBBP/EP3 are critical to sustain the proliferation of human leukemia and lymphoma cell lines. EP3 is very abundant at super-enhancers in K562 and is coincident with sites of GATA1 and MYC occupancy. In accordance, CREBBP/EP3 bromodomain inhibitors interfere with GATA1- and MYC-driven transcription, causing the accumulation of cells in the G/G1 phase of the cell cycle. The CREBBP/CBP3 bromodomain inhibitor CBP3 displaces CREBBP and EP3 from GATA1 and MYC binding sites at enhancers, resulting in a decrease in the levels of histone acetylation at these regulatory regions and consequently reduced gene expression of critical genes controlled by these transcription factors.