In diabetic setting, the activated NF-κB translocates into the nucleus and triggers the expression of its target genes including ICAM-1, MCP-1, and TGF-β1 which in turn induce persistent and enhanced inflammation, and finally lead to excessive fibronectin (FN) production and ECM accumulation resulting in acceleration of the pathogenesis of glomerular sclerosis and tubulointerstitial fibrosis [16]. This evidence concerns the gene NFKB1 and glomerulosclerosis.