AR and posterior cortical atrophy: The gene amplification and some gain-of-function mutations (such as T878A, F877L W742C, L702H, and so on) can lead AR to be activated in the presence of very little androgens, even in the presence of other hormones even drugs (such as progesterone, flutamide, bicalutamide, and enzalutamide) and maintain transcription activity to promote the tumorigenesis and development of PCa [66,67,68].