High levels of R-2-HG also inhibit PHD (prolyl hydroxylases) and the degradation of HIF1-α, favoring tumor formation, growth and survival through the production of vascular endothelial growth factor (VEGF), glucose transporter 1 (GLUT1), phosphoglycerate kinase 1 (PGK1) [158]. The gene discussed is VEGFA; the disease is neoplasm.