The most frequent alterations in gliomas include dysregulation of growth factor signaling via amplification and mutational activation of receptor tyrosine kinase genes such as EGFR. Phosphatidylinositol-3-kinase (PI3K) signaling pathways are also activated due to genetic alteration in the phosphatase and tensin homolog (PTEN) tumor suppressor gene on 10q23.3 at the level of loss of heterozygosity, mutation, and methylation in at least 60% of gliomas [6]. Here, EGFR is linked to glioma.