Interestingly, VEGFR-2− ECs expressed FSP-1 and α-SMA at a higher level and exhibited greater proliferative capacity, compared with those VEGFR-2+ ECs isolated from the same human GBM tumor (Supplementary Fig. 6), implicating that loss of VEGFR-2 expression correlates to EC acquisition of mesenchymal transformation and phenotypes including enhanced proliferation. Here, KDR is linked to glioblastoma.