To address this issue, Junttila et al. and Feldser et al. induced lung adenocarcinoma by simultaneous inactivation of p53 and K-Ras activation, and then restored p53. Importantly, restoration of p53 activity only resulted in the regression of adenocarcinoma and did not affect adenoma.13, 14 In addition, the Arf–p53 pathway was retained in mouse embryonic fibroblast cells expressing K-RasG12D. Here, KRAS is linked to lung adenocarcinoma.