MYC and neoplasm: 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.