In progression of renal-function decline in CKD mammal models, IS not only stimulates nuclear translocation of phosphorylated NF-κB p65 to induce activation of NF-κB signaling [37] but also aggravates renal fibrosis via upregulation of TGF-β1, plasminogen activator inhibitor-1 (PAI-1), the tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), and pro-α1 (I) collagen [38,39] (Figure 2). This evidence concerns the gene NFKB1 and chronic kidney disease.