This, together with higher glucose and lower lactate and alanine levels found in the HIF-2+ tumors (compared to both EV and HIF-1+ tumors), results in a more oxidative, DNA damage-tolerant phenotype that supports enhanced tumor growth, similar to the Sporadic VHL-deficient clinical subtypes of CCRCC described by Gordan et al. [21]. This evidence concerns the gene VHL and nonpapillary renal cell carcinoma.