Rapamycin, which binds the FKBP-rapamycin-binding domain and not the ATP binding pocket, predominantly inhibits mTORC1 complex formation.51 As recent data have demonstrated that mTORC2 is important for HIF-2α protein translation in ccRCC,31, 32 we asked the question of whether HIF-2α ablation by an mTORC1/2 kinase inhibitor, which interacts with the ATP binding pocket of mTOR and thus inhibits both mTORC1 and mTORC2 activity, affected p53 status in ccRCC cells. This evidence concerns the gene TP53 and nonpapillary renal cell carcinoma.