In VHL-mutated ccRCCs, both HIF1α and HIF2α are important, due to the frequent HIF1A deletions (40–55%); furthermore, a murine model demonstrated the sufficient inhibition of ccRCC pathogenesis by Hif2α degradation and the necessity for the ccRCC formation by Hif2α stabilization [46]. Here, HIF1A is linked to nonpapillary renal cell carcinoma.