My original idea was to study a mouse model of lung cancer, which had been used previously to study effects of LKB1 loss, in which an oncogenic mutant of K-Ras was switched on, with or without knockout of LKB1, by administration to the lungs via nasal inhalation of a viral vector expressing Cre recombinase [78]. The gene discussed is STK11; the disease is lung carcinoma.