As expected, our recent study reveal that ERRα, which exhibits an up-regulation expression pattern in metastatic CRPC tissues and also the castration-relapse VCaP-CRPC xenograft model, can function to promote the castration-resistant growth of prostate cancer by enhancing the intratumoral androgen biosynthesis and thus activation of AR signaling via a mechanism of direct transactivation of two key androgen biosynthesis enzyme genes CYP11A1 and AKR1C3 [40]. The gene discussed is CYP11A1; the disease is Familial prostate cancer.