Augmented inflammation is a hallmark of diabetes,81 and this proinflammatory state plays a critical role in the development and progression of DKD.82, 83 Inflammatory factors such as infiltration of macrophage and inflammatory cytokines and chemokines (MCP‐1, IL‐6, TNF‐α, PAI‐1, CXCR4 etc) can activate myofibroblasts at injury sites in the kidney whilst inducing the differentiation of MCs, glomeruli, and renal tubular epithelial cells into fibroblasts, resulting in enhanced ECM production and deposition, which in turn promote fibrosis.84, 85, 86, 87. This evidence concerns the gene CCL2 and diabetic kidney disease.