Other studies have shown that increased circulating FGF-2 levels fails to improve the outcome of lipopolysaccharide (LPS)-induced AKI but leads to further renal damage because circulating FGF-2 may predispose endothelial cells to undergo apoptosis in response to LPS or induce inflammatory changes.43 This was further confirmed by high serum FGF-2 levels in children with sepsis who were at a high risk of developing AKI. The gene discussed is FGF2; the disease is Sepsis.