Because CDK1 is frequently overexpressed or amplified in cancer [68,69,70,71] and expression of the BRD4 target gene MYC is significantly elevated in related cancers such as TNBCs [72], we hypothesize that CDK1 activated in cancers may stimulate BRD4 hyperphosphorylation to support stronger chromatin binding and target oncogene expression, thereby driving tumor growth and BETi resistance. This evidence concerns the gene BRD4 and neoplasm.