Elevated phosphorylation of AKT1/2 is observed in 40–50% of bladder cancer cases, independent of PIK3CA or PTEN alterations, and may result from upstream receptor tyrosine kinase (e.g., FGFR3 or EGFR) activation (10, 17). The gene discussed is FGFR3; the disease is urinary bladder carcinoma.