The resistance of GBM to a range of therapies is mainly due to a highly mutated genome and an overactivation of tyrosine kinase receptors, such as the epidermal growth factor receptor (EGFR), the platelet-derived growth factor receptor (PDGFR), and the vascular endothelial growth factor receptor (VEGFR), which have been found upregulated in GBM [5,6,7,8]. This evidence concerns the gene PDGFRB and glioblastoma.