AKT was not differentially phosphorylated in tumors with and without FGFR3 mutations, suggesting that, in bladder cancer, AKT can be activated by several mechanisms including the aberrant activation of FGFR3, such as EGFR activation in basal tumors (Rebouissou et al, 2014; Fig 3F, right panel). This evidence concerns the gene AKT1 and urinary bladder carcinoma.