Based on the knowledge that KRAS signaling regulates a diverse array of cellular pathways relevant to differentiation [2, 12–15], we hypothesized that, independent of the role of mutant KRAS as a driver mutation for lung cancer, modulation of KRAS expression and/or activity in the normal airway epithelium has a significant influence on normal airway epithelial differentiation and that cigarette smoking, a stress associated with abnormal epithelial differentiation, dysregulates airway epithelial differentiation in part by abnormal activation of KRAS. This evidence concerns the gene KRAS and lung carcinoma.