After AKI, the activation of TLRs by IL-1 and DAMPs can trigger an excessive inflammatory response and facilitate interstitial fibrosis; in contrast, the deletion of Myd88, an TLR/IL-1 downstream protein and an NF-κB upstream protein, ameliorates renal fibrosis after kidney damage [17,166]. This evidence concerns the gene NFKB1 and renal fibrosis.