Several AR mutations have been implicated in therapeutic resistance to ARTA, often through AR activation by glucocorticoids and other sex hormones (e.g. L702H, H875Y) or gain of function mutations that confer AR agonist activity to AR antagonists (e.g., T878A, H875, F877L, W742C) [12, 17], Discrepancies in the current literature, as well as the conflicting results from various genomic analyses, further complicates effective, evidence-based treatment selection among patients with prostate cancer. Here, AR is linked to Familial prostate cancer.