We have specifically demonstrated that knockdown of AR or treatment with AR antagonists considerably inhibits both of them [14,28,29] and that AR signals either activate oncogenic molecules, such as ATF2 [15], β-catenin [30], EGFR/ERK/Akt [11], ELK1 [31], and NF-κB [32], in bladder cancer cells or inactivate tumor suppressors, such as GATA3 [33], FOXO1 [34], and UGT1A [35], in non-neoplastic urothelial cells. The gene discussed is ATF2; the disease is urinary bladder carcinoma.