Recent studies have demonstrated that Fib and its degradation products act as strong mitogens and play a major role in renal interstitial fibrosis in kidney disease by stimulating renal fibroblast proliferation in a dose-dependent manner through TLR2-, TLR4-, and ICAM-1-dependent signaling in unilateral ureteral occlusion (UUO). This evidence concerns the gene TLR2 and kidney disorder.