In previous studies, we demonstrated interactions between CCR2 and MET receptors in the DCIS progression and metabolism.27 In these studies, we showed that HGF and CCL2 cooperated to enhance breast cancer growth, survival, and invasion, induced broad metabolic changes associated with glycolysis, and enhanced p42/44MAPK, AKT and AMPK signaling to regulate glucose metabolism. This evidence concerns the gene CCL2 and ductal breast carcinoma in situ.