Furthermore, it is tempting to speculate that these TPα/TPβ-mediated effects may account, at least in part, for the clinically well-documented observation that during prostate cancer progression, AR-target gene expression is up-regulated even in the absence of testicular androgens or in the presence of AR antagonists, such as in the case of CRPC. The gene discussed is PLAT; the disease is Familial prostate cancer.