Indeed, AKI is often accompanied by the presence of DNA damage [47], which leads to the activation of the ataxia telangiectasia mutated (ATM) and/or ataxia telangiectasia and Rad3-related (ATR) proteins, two phosphaditylinositol 3-kinase family members that phosphorylate several downstream targets, including p53 and checkpoint kinase 2 (CHK2), with consequent production of p21Waf1/Cip1, a cell cycle inhibitor that arrests tubular epithelial cells in the G1 phase or in G2/M phase of cell cycle [47,48]. This evidence concerns the gene TP53 and acute kidney injury.