CDK2 and breast cancer: As our observations in vitro and in vivo clearly demonstrated that CDK2-mediated phosphorylation of EZH2 at T416 is crucial for driving and maintaining the TNBC phenotype (Fig. 1) and that constitutively active CDK2 transgenic mice develop mammary tumors with basal-like phenotype14, we further asked whether blocking the upstream activation of EZH2 by CDK2 inhibitor (CDK2i) can also upregulate ERα.