In addition, we noticed that the type 2A pVHLY98H mutant associated with low risk ccRCC behaved similarly to pVHLR200W Chuvash mutant being partially, but not fully impaired in HIF2α-P-OH peptide binding, reinforcing the role of HIF2α as oncogenic driver in ccRCC (Extended Data Fig. 4h). This evidence concerns the gene EPAS1 and nonpapillary renal cell carcinoma.