To evaluate requirements for Yap in lung tumors induced by activated-Kras, we employed a mouse model for lung adenocarcinoma in which expression of an oncogenic (activated) allele of Kras (KrasG12D) is dependent upon Cre recombinase-mediated excision of a transcriptional terminator from an inactive allele (KrasG12D.LSL), initiated by inhalation of an adenovirus-expressing Cre recombinase [33] (Figure 1B). Here, KRAS is linked to lung adenocarcinoma.