Therefore, Runx3f/f and Runx3f/f;K-RasLSL-G12D/+ mice faithfully recapitulate the development of human lung AAH and adenocarcinoma, respectively.21 Although the specific cells of origin of each type of adenoma remain to be identified, these results clearly demonstrate that inactivation of Runx3 is responsible for the development of multiple types of lung adenomas. This evidence concerns the gene RUNX3 and adenoma.