Since it has been shown that aberrant activation of AR as a result of its interaction with p52 causes the castration-resistant growth of prostate cancer cells in an androgen-deprived environment [10], we studied the effect of the AR/p52 inhibitors on growth of parental androgen-dependent LNCaP and its castration-resistant variant C4-2 human prostate cancer cells under normal physiologic androgen levels (1 to 2 nM synthetic androgen R1881, denoted by +R) [33] compared to very low androgen levels (denoted by −R) conditions. The gene discussed is AR; the disease is prostate cancer.