Together with AR amplification, these missense mutations account for 60% of CRPC oncogenic mutations [37] and function by rendering prostate cancer cells resistant to AR antagonists (e.g., hydroxyflutamide and enzalutamide) or by imposing agonist-bound structural conformations, which lead to the reactivation of AR signaling [38,39]. The gene discussed is AR; the disease is Familial prostate cancer.