The detailed molecular mechanism of class IIa HDACs-mediated these processes may be multifaceted, we demonstrated that TMP269 treatment inhibited the phosphorylation of p53, a well-known tumor suppressor that contributes to AKI by regulating apoptosis and autophagy (Yan et al., 2016; Tang et al., 2019), and preserves expression of E-cadherin, Klotho and BMP-7, three proteins that protect against AKI (Hu and Moe, 2012; Manson et al., 2015; Ma et al., 2017; Gao et al., 2018). The gene discussed is TP53; the disease is acute kidney injury.