As a result of FGFR3 activation, both an increase in MYC mRNA levels due to activation of the p38α MAP kinase and stabilization of the MYC protein mainly due to activation of AKT were reported, and the authors emphasized the vital role of these two pathways in MYC accumulation in bladder cancer with aberrantly activated FGFR3 [91]. This evidence concerns the gene AKT1 and urinary bladder cancer.