Several molecular mechanisms have been identified to aberrantly activate the Akt kinase signaling pathway in bladder cancers, including: (1) mutations of upstream activators, such as p110α (PIK3CA), FGFR3 and Ras[21]–[24]; (2) activating mutations of the Akt kinase [25], and (3) loss of heterozygosity (LOH), homozygous deletion and inactivating mutations of the negative regulator PTEN[26]–[29]. Here, FGFR3 is linked to urinary bladder carcinoma.