Several mechanisms, including hemodynamic malfunction, hyperglycemia, glycosylation of non-enzymatic protein, and aberrant metabolism of cellular glucose, have a crucial role in the pathogenesis of DN, which lead to activation and release of IL-6 and TNF-α and reduction of IL-10 in the kidney tissue, which finally causes the accumulation and deposition of extracellular matrix in the glomerular mesangium [35]. This evidence concerns the gene TNF and liver dysplastic nodule.