Thus, inactivation of VHL in RCC is associated with increased levels of HIF-α isoforms and a subsequent increase in hypoxia-inducible genes, such as those involved in angiogenesis (VEGF, PDGF), erythropoiesis (EPO), glycolysis (Glut1), cell growth and survival (Cyclin G2, TGF-α), and cell migration (CXCR4), suggesting that the genes upregulated by the VHL-HIF pathway are involved in the progression of renal cell carcinoma [8,13,15]. This evidence concerns the gene VHL and renal cell carcinoma.