Regardless of duration of the disease process, DM patients have been found to have abnormal expression of NF-κB in vivo, suggesting that NF-κB is an important pathogenic factor in the occurrence and development of DN [9,10,11], therefore, the inhibition of NF-κB might have a substantial protective effect in DN, and the NF-κB signaling pathway, including MCP-1, TGF-β1 and FN, might be an important target to the treatment of this disorder [12,13]. The gene discussed is CCL2; the disease is liver dysplastic nodule.