These new data provide additional knowledge of androgen-independent prostate cancer progression compared to previous studies, which primarily focused on changes in AR ligand binding specificity that may result from gene structure changes (e.g., mutation, amplification, or spliced variant expression) or AR ligand-independent activation arising from alternative signal pathways that activate AR activity at the castration level of androgen (2,24). This evidence concerns the gene AR and Familial prostate cancer.