For example, mutations in KRAS[3] and in the epidermal growth factor receptor (EGFR) [4] typically occur early in the development of lung adenocarcinomas, whereas amplification of EGFR and PI3KCA[2] and epigenetic inactivation of the p16 tumor suppressor [5] are more frequent in SCC pathogenesis relative to adenocarcinomas. This evidence concerns the gene EGFR and lung adenocarcinoma.