Concerning the molecular mechanisms underlying short- and long-term renal dysfunction/nephrotoxicity, previous reports have suggested a close link between severe glomerular and tubular lesions (including atrophy, fibrosis, inflammation and sclerosis) and increased mediators of inflammatory response, with activation of NF-κB and increased TGF-β1 release, which then causes nephropathy mediated by fibrosis and apoptosis of renal cells [40–42]. Here, NFKB1 is linked to Nephropathy.