For instance, primary GBM is characterized by epidermal growth factor receptor (EGFR) gene amplification and mutations, the loss of heterozygosity (LOH) of chromosome 10q containing phosphatase and tensin homolog (PTEN), the overexpression of mouse double minute 2 (MDM2), and the deletion of the p16 tumor suppressor gene [13]. The gene discussed is EGFR; the disease is glioblastoma.