The EGFR gene mutation and amplification, the overexpression of mouse double minute 2 (MDM2), the deletion of p16, the loss of heterozygosity (LOH) of chromosome 10q harboring phosphatase and tensin homolog (PTEN) [15], and the mutation of the TERT promoter are all hallmark abnormalities of primary GBM. Here, PTEN is linked to glioblastoma.