Improvements in our understanding of the molecular mechanisms underlying the oncogenic activity of activated FGFR3 in bladder tumors may facilitate the identification of new drug targets that could be acted on together with FGFR3, to increase the efficacy of anti‐FGFR3 therapies and/or to prevent potential drug resistance. The gene discussed is FGFR3; the disease is urinary bladder neoplasm.