Furthermore, co-treatment of tumor ECs with VEGFR-2 inhibitor Ki8751 (IC50 = 0.9 nM) and PDGFR inhibitor crenolanib (IC50 = 0.9 and 1.8 nM for PDGFR-α and PDGFR-β, respectively) inhibited EC viability in a dose-dependent manner (Fig. 5d), suggesting that PDGFR inhibition sensitizes GBM ECs to anti-VEGF treatment. This evidence concerns the gene VEGFA and glioblastoma.