PCa was originally identified as an androgen‐dependent tumor, and its growth and survival were found to be controlled by AR signaling.4 Androgen deprivation therapy is effective for inhibiting PCa growth by initially suppressing AR activity.5 However, this treatment is more likely to lead to recurrence of prostate cancer, and relapsed prostate cancer is not responsive to androgen deprivation therapy.6 Despite the loss of response to antiandrogens, data suggest that AR signaling continues to play a role in castration‐resistant prostate cancer. This evidence concerns the gene AR and posterior cortical atrophy.