Recently, C-reactive protein (CRP) has been found to trigger a novel NF-κB-involved signaling pathway in the progression of DN, more narrowly, in human CRP transfected-db/db mice and cultured renal tubular epithelial cells, CRP is proved to promote inflammation via the evoking and dimerization of dipeptidyl peptidase-4 (DPP4) through DPP4/CD32b/NF-kB signaling circuit. The gene discussed is CRP; the disease is liver dysplastic nodule.