EGFR is overexpressed in more than 60% of NSCLC cases and considered as a driving force in lung adenocarcinomas [3], so targeting EGFR to inhibit EGFR-mediated pro-survival and anti-apoptotic signals through the MAPK/ERK and PI3K/AKT pathways would be an effective lung cancer treatment. This evidence concerns the gene AKT1 and lung adenocarcinoma.