Primary GBM (~90% of cases) is commonly characterized by the amplification of the epidermal growth factor receptor (EGFR) [9] and deletion of the phosphatase and tensin homolog (PTEN) [10], while secondary GBM (progressed from lower grade gliomas) is more often associated with mutations of the Tumor Protein p53 (TP53) and isocitrate dehydrogenase 1 (IDH1) [11, 12] (Figure 1). This evidence concerns the gene PTEN and glioblastoma.