Cross-talk occurs between ER and NF-κB in breast cancer which is mediated by estradiol and TNF-α; the combined activity of the estrogen and inflammatory cytokine promotes the transition of breast cancer cells to a more aggressive, ER-positive but antiestrogen-resistant phenotype with constitutive activation of NF-κB and an increased propensity for distant metastasis [110]. This evidence concerns the gene ESR1 and breast carcinoma.