Loss of VHL function due to VHL gene mutation results in the accumulation of HIF, which then induces the over-expression of hypoxia related genes including erythropoietin (Epo) [6], vascular endothelial growth factor (VEGF) [7], [8] and platelet-derived growth factor (PDGF) [9], thus promoting angiogenesis, proliferation and tumorigenesis in multiple organs such as hemangioblastoma in brain and retina, renal cell carcinoma and cyst, pheochromocytoma, pancreatic cyst and tumor. This evidence concerns the gene VHL and hereditary pheochromocytoma-paraganglioma.