In UBC, two FGFR3-involved mechanisms may account for the tumor genesis [9, 10, 58]: first, the somatic point mutation within the FGFR3 creates a cysteine residue in the extracellular region, and gives rise to the receptor dimerization via the intermolecular disulphide bond formation followed by the ligand-independent receptor activation [59, 60]; Second, the overexpression of a wild-type receptor, which is more frequently observed in higher grade tumors. Here, FGFR3 is linked to neoplasm.