Studies have shown that gliomas lack mutations in the EGFR exons 19–21 encoding the tyrosine kinase domain (common activating mutations in lung cancer that sensitize those cancers for gefitinib and erlotinib), and may be less dependent on EGFR kinase activity overall, also contributing to the failure of EGFR-TKIs [51]. This evidence concerns the gene EGFR and glioma.