Previous work indicates increases in metabolic pathways in the airways of subjects with dysplastic lesions14, in PMLs adjacent to LUSC tumor24, and in smokers at high-risk for lung cancer25 as well as increases in proliferation (via Ki67 levels, as mentioned above) that have been utilized as an endpoint in lung cancer chemoprevention26,27. The gene discussed is MKI67; the disease is lung carcinoma.