In AKI, obstructive renal injury, and diabetic nephropathy, epigenetic modifications induced an increase in proinflammatory and profibrotic cytokines such as monocyte chemoattractant protein-1 (MCP-1), complement protein 3 (C3), transforming growth factor β (TGF-β), which in turn perpetuate inflammation and promote epithelial-to-mesenchymal transition (EMT) that contributes to renal fibrosis34–38. This evidence concerns the gene CCL2 and diabetic kidney disease.