Recent data indicated that VEGF, an angiogenic growth factor known to be overexpressed in GBM, promoted the endocytosis of endothelial cell adhesion molecule VE-cadherin and the down-regulation of TJs proteins (including Claudin-5, Occludin, ZO-1), resulting in the disruption of BBB function and increased endothelial permeability [37,38]. The gene discussed is CLDN5; the disease is glioblastoma.