VEGFA and glioblastoma: Then, we investigated the underlying mechanisms by which M2 macrophage promoted GBM aggressiveness, and we expectedly found that M2 macrophages VEGF-dependently promoted cell proliferation, epithelial-mesenchymal transition, tumorigenesis, and angiogenesis, which were supported by the existed data that VEGF itself serves as an oncogene in GBM [43, 44].