In both cohorts, EUR ccRCC tumors were enriched in inflammatory pathways (IFN-α and IFN-γ response, allograft rejection), proliferative pathways (E2F targets, G2–M checkpoint, Myc signaling), metabolic pathways (glycolysis, oxidative phosphorylation, fatty acid metabolism, bile acid metabolism, peroxisome, and MTORC1 signaling), and the unfolded protein response. This evidence concerns the gene MYC and nonpapillary renal cell carcinoma.