Collective efforts to classify the pathogenesis of gliomas have shown that GBM frequently harbors a signature of mutations that tend to attenuate the function of tumor suppressor genes, such as p53 and PTEN, or enhance activation of receptor tyrosine kinases such as epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor (PDGFR) (reviewed in [3],[4]). This evidence concerns the gene EGFR and glioma.