For instance, redox-protective proteins such as SOD2 were reduced by androgen deprivation in castration-resistant prostate cancer cells [113,114], yet SOD2 repression contributed to the castration resistance of prostate cancer cells via AR reactivation through various mechanisms, including inducing the expression of genes involved in steroid metabolism, such as AKR1C3 [115], and genes encoding nuclear receptor co-regulators, such as NCOA4 [116]. The gene discussed is NCOA4; the disease is prostate carcinoma.