This combination significantly extends survival in both models and involves multifaceted anti-tumor activities including: direct oncolysis of tumor cells, extensive tumor apoptosis and necrosis, increased macrophage infiltration to the tumor, greatly reduced tumor vascularity (i.e., CD34+ blood vessels) and inhibition of angiogenic PDGFR/ERK pathway in patient GSC-derived GBM model, and T cell dependent activity in mouse GSC-derived GBM model (Figure 5) [76]. This evidence concerns the gene PDGFRB and glioblastoma.