Targeting the perivascular niche, through antiangiogenic therapies, represents a promising approach to prevent tumor progression, but the adoption of VEGF antagonism (bevacizumab) is insufficient to inhibit the formation of new GBM stem cell niche, as it seems to increase the expression of proangiogenic factors as FGF1 and FGF2 and CXCL12 [84, 85] and the recruitment of proangiogenic bone-marrow derived cells [86]. Here, VEGFA is linked to glioblastoma.