In ovarian cancer, BRD4 inhibition was shown to reprogram tumor-infiltrating macrophages from the M2-type to M1-type, promoting proinflammatory cytokine secretion and the subsequent activation of CD8+ T cells [85], and, in prostate cancer, BRD4 inhibition was associated with an increased expression of MHC 1 genes by tumor cells, modification of the global gene expression with an activation of antigen-processing networks and an increased CD8+ T cells/Tregs ratio [86]. This evidence concerns the gene CD8A and ovarian carcinoma.