Intriguingly, in prostate cancer patients treated with the nonspecific P450c17 inhibitor, ketoconazole, or the specific P450c17 inhibitor, abiraterone acetate, significant (∼20 μg/dL) circulating DHEAS concentrations were still present, suggesting that this could act as a depot for further downstream androgen formation via desulfation and AKR1C3 action (319). The gene discussed is CYP17A1; the disease is Familial prostate cancer.