Thus, the pathogenesis of DN via increased vascular inflammation and fibrosis has implicated inflammatory cells, cytokines, and profibrotic growth factors such as transforming growth factor-β (TGF-β), monocyte chemoattractant protein-1 (MCP-1), interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-18 (IL-18), among others [7]. This evidence concerns the gene CCL2 and liver dysplastic nodule.