To determine the selective effects of mutational activation of KRAS on these proteins in lung adenocarcinomas, we compared KRAS-mutant tumors (n = 75) to other tumors with wild-type KRAS. We further divided tumors with wild-type KRAS into those with other mutations in components of the mitogenic RTK/RAF/MAPK pathway and those without, using the criteria found in the TCGA publication16. The gene discussed is KRAS; the disease is lung adenocarcinoma.