This is supported by our observations that: (1) Cisplatin-associated AKI was accompanied by decreased E-cadherin expression while MLL1/WDR5 inhibition resumed E-cadherin expression and renoprotection; (2) Inhibition of MLL1/WDR5-mediated p53 phosphorylation promoted cell survival and retained E-cadherin expression in cultured RPTCs exposed to cisplatin; (3) Silencing E-cadherin counteracted the protective effect of MLL1/WDR5 inhibition. The gene discussed is TP53; the disease is acute kidney injury.