Moreover, recent studies have demonstrated that KDR activation through sustained VEGF-C promotes GBM maintenance and growth even under bevacizumab therapy, meaning that activation of KDR through VEGF-C is an escape mechanism of GBM to overcome bevacizumab therapy.40 The proliferative effects of KDR activation in GBM occur with the binding of both VEGF-A and VEGF-C ligands, though it should be noted that the effects of these 2 VEGF ligands have been demonstrated to be non-overlapping (Figure 5). This evidence concerns the gene VEGFC and glioblastoma.