Consistent with previous reports of a pro-tumorigenic role of NOS in lung cancer [6–9], we demonstrate that in a genetically engineered mouse model of Kras-driven NSCLC, L-NAME treatment inhibits lung tumor growth, reduces tumor burden, increases median OS, and improves HR, even when treatment is initiated in the presence of established disease. This evidence concerns the gene NOS2 and non-small cell lung carcinoma.