Metastatic prostate cancer usually responds initially to medical or surgical castration, then eventually progresses as castration-resistant prostate cancer (CRPC), which is stimulated by intratumoral synthesis of testosterone and/or 5α-dihydrotestosterone (DHT) and activation of the androgen receptor (AR) (Attard et al., 2016; Chang et al., 2013; Mostaghel et al., 2014; Scher and Sawyers, 2005; Hearn et al., 2016). Here, AR is linked to metastatic prostate carcinoma.