Over the last few years, it has become increasingly well recognized that in addition to point mutations, alternative splicing events that lead to constitutively active AR variants (AR-Vs) are another clinically relevant means by which prostate cancer is able to progress in spite of agents that effectively disrupt the AR-ligand interaction (Fig. 1) [9, 20, 25, 31, 53–55, 69]. The gene discussed is AR; the disease is Familial prostate cancer.