The potential of IL–6 of inducing and maintaining EMT in breast cancer cell lines depends on the activation of the JAK2/STAT3 pathway or tropomyosin receptor kinase C (TrkC) that triggers EMT and activates Twist1-mediated IL–6 overexpression, securing the EMT phenotype via a feedback loop interaction [38,43]. This evidence concerns the gene STAT3 and breast carcinoma.