Furthermore, the most salient characteristic of the VHL mutant cells is the hypoxic response induced by the stabilization of HIF-α, which results in tumor angiogenesis [via overexpression of vascular endothelial growth factor (VEGF) and Oncostatin M (OSM)] and metabolic switch (via reduced oxidative phosphorylation-based respiration) [23, 135, 136]. This evidence concerns the gene VHL and neoplasm.