We used a well-established LSL-KrasG12D (Lox-STOP-Lox KrasG12D) lung tumorigenesis model, in which mutant KrasG12D is activated by Cre recombinase via intratracheal instillation of Cre-expressing adenovirus (Ad-Cre) to delete the STOP element, leading to sequential development of epithelial hyperplasia, adenomas, and eventually adenocarcinomas in the lung (46). The gene discussed is MAP6; the disease is adenoma.