These aberrant molecules, including 1p and 19q co-deletions (oligodendroglioma-specific), IDH gene mutations, PTEN (Phosphatase and tensin homolog) gene mutations, TP53 mutations, TERT (Telomerase reverse transcriptase) gene promoter mutations, ATRX (Alpha thalassemia/mental retardation syndrome X-linked) gene mutations, and EGFR (Epithelial growth factor receptor) gene amplification, are forcing clinicians to reconsider traditional GBM treatment (Mclendon et al., 2008; Brennan et al., 2013). This evidence concerns the gene PTEN and oligodendroglioma.