Given that the incidence of certain somatic driver mutations in lung adenocarcinomas differs in smokers and non-smokers, for instance, lung tumours of never smokers have more EGFR mutations but fewer KRAS mutations compared with tumours from smokers21, 22, we hypothesize that ZEB1 exerts a growth suppressive role that is genetic context dependent. Here, EGFR is linked to lung adenocarcinoma.