In U87-MG cells baseline levels of some VEGF isoforms under normoxia, mainly VEGF189 were high due to hypoxia-independent mechanisms as reactive oxygen species [21], NO [22], phosphatidylinositol-3-kinase and MAP kinase activation through the action of mTOR [23], or loss of IDH1 gene function in glioblastoma [9]. This evidence concerns the gene IDH1 and glioblastoma.