The loss or inactivation of pVHL function in ccRCC leads to a state of “pseudohypoxia” where stabilized HIF-1α and HIF-2α induce the transcription of hypoxia responsive genes, resulting in alterations such as increased glucose and ribose metabolism, pH deregulation, cell proliferation, and angiogenesis, giving ccRCC a high metastatic potential [1,9,12,13,14]. This evidence concerns the gene EPAS1 and nonpapillary renal cell carcinoma.