In bladder cancer, FGFR3 activation further intersects with IFN-γ signaling by modulating PD-L1 stability through NEDD4-dependent ubiquitination or by altering IFN-γ-induced PD-L1 turnover in FGFR3-TACC3 fusion models [138,139]. This evidence concerns the gene FGFR3 and urinary bladder carcinoma.