Given our observations that CDK1 inhibition prevents BRD4 hyperphosphorylation and that CDK1-mediated mitotic hyperphosphorylation of BRD4 contributes to BETi resistance (Figure 4E), we reasoned that CDK1 inhibitors used in combination with BETis may be able to generate a synergistic effect in suppressing cancer cell proliferation. Here, CDK1 is linked to cancer.