Lin et al. noticed that TLR4 was up-regulated in renal tubules of human kidneys with diabetic nephropathy and high glucose induced TLR4 expression via protein kinase C activation, resulting in up-regulation of IL-6 and chemokine (C-C motif) ligand 2 (CCL-2) by IκB/NF-κB activation in human tubular epithelial cells, contributing to tubulointerstitial inflammation in DN [12]. This evidence concerns the gene CCL2 and diabetic kidney disease.