These observations might explain the rapid recurrence of K-Ras-induced lung cancers with secondary oncogene activation after initial regression due to K-Ras suppression: inhibition of oncogenic K-Ras causes the cancer to regress; however, K-Ras mutation-free AD cells are resistant to the inhibition and are cancer-prone because their Arf-p53 pathway (oncogene surveillance mechanism) is suppressed through Runx3 inactivation. Here, CDKN2A is linked to lung cancer.