Therefore, both the genetic manipulation of Akt1 in the SPC-IGFIR transgenic mice and the use of a selective AKT1 inhibitor in human lung cancer cell lines suggests that AKT1 is a critical regulator of lung adenocarcinoma development, particularly in tumor cells containing wild type p53. Currently only the MK-2206 is being evaluated in clinical trials and our data suggests that AKT1 selective inhibitors may warrant evaluation in clinical trials, at least for lung adenocarcinomas expressing wild type p53. This evidence concerns the gene IGF1R and lung adenocarcinoma.