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, consequently, the tumor formation capacity of breast cancer cells. This evidence concerns the gene KDM4B and neoplasm.