We utilized an autochthonous mouse model of ALK+ NSCLC as a model system, in which intrapulmonary administration of an adenovirus encoding two guide RNAs and Cas9 resulted in oncogenic rearrangement of the Eml4 and Alk genes (Fig. 2a), leading to the formation of lung tumors that histologically resembled human lung adenocarcinoma25. This evidence concerns the gene ALK and non-small cell lung carcinoma.