KDR and glioblastoma: Previous attempts to restrain GBM growth targeting VEGF or its receptors, either by bevacizumab (a humanized monoclonal antibody specific for VEGF), by VEGF-trap (a soluble decoy receptor for VEGF) or by anti-VEGFR antibody, resulted in the improvement of tumor cells’ ability to invade brain parenchyma, a phenotypic change known as infiltrative shift [35,36,37].