Genomic mechanisms for activating the EGFR gene include nucleotide substitutions and in-frame insertions/deletions of the kinase domain in lung adenocarcinoma and papillary thyroid carcinomas, and multi-exonic deletions (exons 2 through 7: EGFR variant III or vIII), nucleotide substitutions of the extracellular domain and carboxyl terminal deletions in glioblastoma[2-6]. This evidence concerns the gene EGFR and thyroid gland papillary carcinoma.