Therefore, our results, taken together with another previously published report, indicate that IKKα in lung epithelial cells can function as an evolutionarily conserved NSCLC tumor suppressor by multiple independent mechanisms (ROS up-regulation and/or HIF-1α up-regulation and activation), suggesting that the mechanisms whereby IKKα functions as an NSCLC suppressor may depend on the nature of the oncogenic mutations responsible for the development and growth of specific NSCLCs. This evidence concerns the gene HIF1A and non-small cell lung carcinoma.