The BTB may be characterized by an inflammatory environment with increased numbers of activated astrocytes, vascular endothelial growth factor (VEGF)-induced reduction in the expression of tight junction proteins like claudin-5, breakdown of the basal lamina, and tumor cell interference in associations between endothelial cells and astrocytic endfeet (Figure 2) [15,16,17]. This evidence concerns the gene VEGFA and neoplasm.