This study uncovers an unexpected mechanism by which inflammatory signals influence gene expression in breast cancer cells by regulating the transcriptional activity of the nuclear receptor corepressor (NCoR)/silencing mediator of retinoic acid and thyroid hormone receptor (SMRT)/histone deacetylase 3 (HDAC3) corepressor complex through tumor necrosis factor receptor-associated factor 6 (TRAF6)-dependent ubiquitination events. This evidence concerns the gene NCOR2 and breast cancer.