Preclinical studies suggest that although proliferation of these tumors is primarily CDK4/6-dependent, resistance to CDK4/6i monotherapy might be driven by CDK2 activity (13, 19), and clinical data has shown a correlation between high tumor CCNE1 mRNA levels and impaired response to combined CDK4/6i +/- ET (12, 31). This evidence concerns the gene CDK2 and neoplasm.