Thus, the increased Ang‐2 protein levels in vessels that remained upon bevacizumab therapy further identify Ang‐2 as a potential contributor to therapy resistance/relapse following anti‐VEGF therapy in GBM, a concept that only recently arose from findings in models of pancreatic neuroendocrine tumors (Rigamonti et al, 2014), brain cancer metastasis (Avraham et al, 2014), and U87 xenografts (Burrell et al, 2014). This evidence concerns the gene VEGFA and pancreatic neuroendocrine tumor.