ChIP analysis showed that knockdown of KMT2B reduced H3K4 methylation, and abrogated the recruitment of ERα to cis-regulatory elements adjacent the promoter regions of the ER-target genes IL-20, BCL2, TFF1, and GREB1. Further investigation using whole-genome approaches is necessary to fully elucidate the roles of KMT2B and IL-20 in breast cancer carcinogenesis. This evidence concerns the gene KMT2B and breast cancer.