Some of the observed alterations have been previously identified in different tissue types, such as the downregulation of CCR2, which has been explained by the ability of metformin to block M2-like polarization of tumor-associated macrophages providing the anti-metastatic effect of the drug [41], or downregulation of CYP1B1 in breast cancer cells where due to its crucial role in estrogen metabolism, metformin has been suggested as a potential chemopreventive agent against carcinogenesis [42]. The gene discussed is CCR2; the disease is breast carcinoma.