These results suggest that, in bladder cancer, MAPK kinase phosphorylation could be a marker for resistance while GSK-3β activation or cyclin D1 levels could be a marker for sensitivity of EGFR drug treatment, and that inhibition of both EGFR and PDGFR-β would be more effective in treatment of EGFR-positive bladder cancers than EGFR alone. The gene discussed is GSK3B; the disease is urinary bladder carcinoma.