GBM has two origins: primary GBM (i.e., tumors occurring de novo) representing 90–95% of all GBMs, the remaining 5–10% cases are secondarily originating from low-grade tumors, occurring due to multiple genetic mutations in vascular endothelial growth factor receptor (VEGFR), retinoblastoma protein (RB), phosphatase tensin homolog (PTEN) and several other mutations, causing p53inhibition, amplifying platelet-derived growth factor receptor-α (PDGFRα) and overexpressing cyclin-dependent kinase 4 (CDK4) [6]. Here, PDGFRA is linked to glioblastoma.