In FH-deficient kidney cancer cells, increased fumarate inactivate prolyl hydroxylases, leading to stabilization of HIF, and increased HIF target genes such as GLUT1, vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and transforming growth factor (TGF)α, which facilitate tumor growth [7, 16]. The gene discussed is FH; the disease is neoplasm.