Studies in animal models of diabetes have contributed to defining intracellular and molecular pathways driving renal fibrosis, which include the activation of the renin–angiotensin system, protein kinase C, TGF-β1 and monocyte chemoattractant protein-1 (MCP-1) and the upregulation of plasminogen activator inhibitor-1 (PAI-1), connective tissue growth factor (CTGF)/CCN2, collagen and cytokines [8–11]. This evidence concerns the gene CCL2 and renal fibrosis.