To confirm this hypothesis, we observed a reduction in CBX2 expression upon knockdown of USP27X in BC cells (Fig. 2A and Supplementary Fig. 2A–C), while overexpression of wild-type but not catalytically inactive mutant USP27X C87A (a catalytically inactive point-mutant) resulted in an increase in CBX2 expression in BT549 and HEK-293T cells (Fig. 2B, C). This evidence concerns the gene USP27X and breast cancer.