Notably, in keeping with the crucial role of CDK6 in determining cellular sensitivity of breast cancer cells to CDK4/6i treatment, employment of CK1ε inhibitor D 4476 potentiated the suppressing efficacy of ribociclib on RB1 phosphorylation in MDA-MB-231 cells (Fig. 5f), which was similar with the results we observed in CDK6 knockout cells (Fig. 5g), indicating a functional crosstalk between CK1ε suppression and CDK6 down-regulation. This evidence concerns the gene CDK4 and breast cancer.