Vatalanib treatment induced hypoxia and was associated with the increased expression of several pro-angiogenic cytokines and chemokines such as VEGF, SDF-1, HIF-1α, FGF-1, FGF-2, Ephrin (Eph)-A1, Eph-A2, Angiopoietin-1, and their corresponding receptors VEGFR2, VEGFR3 and EGFR at the tumor-invading front of GBM [31]. The gene discussed is CXCL12; the disease is neoplasm.