Drug-mediated downregulation of multiple Hsp90 protein clients in bladder cancer cellular environments resulted in cell cycle arrest, disruption of tumorigenic signal transduction integrity, and impairment of cell motility and invasion mechanisms, whereas cell death programs in the form of apoptosis and autophagy were strongly activated in response to geldanamycin. The gene discussed is HSP90AA1; the disease is urinary bladder carcinoma.