Several variants, mutations, or even genomic rearrangements (TMPRSS2-ERG fusion is the most common in human prostate cancer, but is absent in small cell carcinoma of the bladder) are involved in pathophysiological situations correlated with AR signaling pathways; the complex interaction of each protein in a specific context may lead to different results, and represents a new pharmacological target for these pathologies, including bladder cancer [29]. Here, AR is linked to urinary bladder carcinoma.