JMJD2B which interacts with ERα and components of the SWI/SNF-B chromatin remodeling complex was recruited to ERα target sites, demethylated H3K9me3 and facilitated transcription of ER responsive oncogenes including MYB, MYC and CCND1, and knockdown of JMJD2B severely impaired estrogen induced cell proliferation and the tumor formation capacity of breast cancer cells as a consequence [27]. This evidence concerns the gene CCND1 and breast carcinoma.