The growth of GBM is angiogenesis-dependent, therefore several antitumor therapies are focused against this process, trying to interfere with molecules that participate in this process, such as hypoxia inducible factor 1 alpha (HIF-1alpha), vascular endothelial growth factor (VEGF) or its receptors (VEGFR2, VEGFR1), erythropoietin (EPO) and endothelial nitric oxide synthase (eNOS) [2, 3]. The gene discussed is EPO; the disease is glioblastoma.