Surprisingly, in breast cancer, ERα, β-catenin and EZH2 interact and target oncogenes, such as c-Myc and Cyclin D1, acting as transcriptional co-activators.169 Furthermore, the redistribution of PRC1 leads to its association with active enhancers enriched for the H3K4me1 mark.139 RING1B was proposed to facilitate ERα recruitment to enhancers and super-enhancers, as well as to promoters of cancer-related genes139,170 (Fig. 4e). This evidence concerns the gene ESR1 and breast carcinoma.