Although subsequent studies found that EGFR and some ligand growth factors were overexpressed in human tumors and the EGFR gene is amplified or rearranged in brain tumors, frequent oncogenic point mutants of EGFR have been first identified in 2004, in human non-small cell lung cancer (NSCLC) from patients who were sensitive to EGFR-specific tyrosine kinase inhibitors (TKIs; e.g., gefitinib and erlotinib) [4,5,6]. This evidence concerns the gene EGFR and brain neoplasm.