In recent studies, we demonstrated that CCL2 induces interactions between CCR2 and MET RTKs, independently of HGF expression, to regulate breast cancer cell growth, survival, and invasion.27 Although CCL2 and HGF are over-expressed in breast cancers,16,28 it remains unclear how CCL2 and HGF function together to regulate breast cancer progression. This evidence concerns the gene HGF and breast carcinoma.