As an E3 ubiquitin ligase, inactivating the VHL gene increased the stability of α-subunits of oxygen-dependent hypoxia-inducible factor (HIF), promoted the constitutive expression of HIF-1α and HIF-2α, and further induced the activation of hypoxia-related genes, such as VEGF, thus promoting tumor progression [8, 9]. This evidence concerns the gene EPAS1 and neoplasm.