Although we and others have previously shown that bradykinin up-regulated IL-6, CCL-2 and TGF expression in cultured PTEC [9] and the application of aprotinin, the KLK inhibitor, improved renal function of STZ-induced diabetic mice [35], the role of KKS in inflammatory pathways leading to DN is still controversial. The gene discussed is CCL2; the disease is liver dysplastic nodule.