It is common knowledge (i) that the prostate is an androgen-addicted organ, (ii) that recurrent PCa, presenting as localized recurrence and/or distant metastatic disease, retains androgen dependence, and (iii) that PCa evades therapy using mechanisms that amplify testosterone uptake, increase sensitivity to testosterone or its metabolites, circumvent AR, or combine the three mechanisms. The gene discussed is AR; the disease is posterior cortical atrophy.