Taken together, these findings provide putative mechanistic links between FGFR3 and IFNG signaling and suggest that FGFR3 inhibition potentially remodels the immune contexture of UTUC by upregulating interferon response genes to reverse its T-cell-depleted phenotype. The gene discussed is FGFR3; the disease is renal pelvis/ureter urothelial carcinoma.