The key regulatory mechanism of BRD4 is the promotion of c-MYC transcription.4,5,80,81 The analysis of genetic mutations in primary, metastatic, or recurrent ovarian cancers has shown that c-MYC gains are potential targets of BET inhibitors.82,83 Additionally, BRD4 plays a significant role in several cellular processes, such as cell differentiation, signal transmission, control of proto-oncogenes, modulation of the cellular cycle, and other pathophysiological processes through non-histone acetylation modifications. This evidence concerns the gene DNER and ovarian cancer.