FGFR3 may be a regulator of the UTUC immune environment by weakening interferon γ (IFNG) signalling, and it is suggested that interferon response genes may be upregulated by inhibiting FGFR3 or PD-1/PD-L1, thereby reversing T cell depletion in UTUC and remodelling the immune environment, which provides a theoretical basis for targeted therapy. This evidence concerns the gene IFNG and renal pelvis/ureter urothelial carcinoma.