To determine the effects of loss of progressively more wild-type Ras genes on carcinogen-induced lung tumorigenesis, mice lacking different combinations of wild-type Hras and Nras alleles were administered the chemical carcinogen urethane, which is well established to induced Kras mutation-positive lung adenomas and adenocarcinomas by 9 to 12 months [13, 15, 17]. The gene discussed is NRAS; the disease is lung adenoma.