Neoangiogenesis, a characteristic histopathologic feature of GBM, is in part secondary to the hypoxic tumor microenvironment that induces hypoxia-inducible factor-1α (HIF-1α) followed by subsequent VEGF accumulation, RTK activation, fibroblast growth factor (FGF), PDGF, hepatocyte growth factor (HGF, also known as scatter factor), integrins, angiopoietins, and STAT3 upregulation [14, 27]. The gene discussed is VEGFA; the disease is glioblastoma.