Mutations in the phosphatase and tensin homolog (PTEN) gene, upregulation of the epidermal growth factor receptor (EGFR), and deletion of chromosome 10q are among the genetic alterations that are prevalent in primary GBM [10], while secondary GBM is frequently associated with chromosome 19q deletion, Isocitrate Dehydrogenase 1 (IDH1) mutation, and Tumor Protein p53 (P53) mutation [9,11]. This evidence concerns the gene PTEN and glioblastoma.