Finally, our results provide in vitro and in vivo proof of concept in xenografts that the inhibition of MYC expression, and, in turn, of FGFR3 expression, by an inhibitor of AKT or p38 or a BET bromodomain inhibitor (JQ1) is a potentially effective strategy for the treatment of FGFR3‐dependent bladder tumors. The gene discussed is AKT1; the disease is urinary bladder neoplasm.