These nuclear export mechanisms of p53 provide a practical future approach to a possible C-PE-induced activation of anti-cancer therapy by p53 [34], as evidenced by the lack of histological irregularities in the C-PE control group as well as the capacity of C-PE treatment of AKI mice to prevent oxidative stress, ER stress, and alterations in the redox environment and cell death markers. The gene discussed is TP53; the disease is cancer.