Because animal models of glomerulosclerosis treated with 17β-estradiol (Maric et al., 2004) or pioglitazone (Nemeth et al., 2019) exhibit reduced tubulointerstitial fibrosis, estrogen and PPAR-γ cell signals may regulate CKD pathogenesis by inhibiting canonical NF-κB signaling. This evidence concerns the gene NFKB1 and chronic kidney disease.