Although our knowledge about the complex network of GBM oncogenic pathways has led to the testing of small-molecule inhibitors or antibodies directed against receptor tyrosine kinases (RTKs; e.g., Ras/MAP/ERK, VEGFR, EGFR, c-Met) or RTK downstream signaling pathways (e.g., PI3K/AKT/mTOR), these treatments have essentially produced disappointing results [3,4]. This evidence concerns the gene KDR and glioblastoma.