We previously demonstrated that infecting the lungs of adult mice with recombinant adenoviral vectors expressing Cas9 and two guide RNAs targeting the relevant intronic regions on Chromosome 17 is sufficient to generate the Eml4-Alk chromosomal inversion and promote the formation of lung adenocarcinomas that closely recapitulate the histological and biological features of human EML4-ALK-driven lung cancers10. The gene discussed is ALK; the disease is lung adenocarcinoma.