Of note, Ang-2 has been shown to be upregulated in the activated endothelium in stroke and glioblastoma models in rodents as well as in glioblastoma patients [7, 32, 52, 57], suggesting that therapeutic interference with Ang-2/Tie2 signaling may be particularly useful to prevent BBB disruption in those disorders. This evidence concerns the gene TEK and glioblastoma.