Mitogen-inducible gene 6 (Mig-6) encodes a widely expressed adaptor protein that negatively regulates EGF signalling, and about half of all mutant mice that lack Mig-6 (Mig-6-/-) die shortly after birth for unknown reasons. Now, Francesco DeMayo and co-workers identify lung defects as a likely cause of these deaths (see p. 3347). The lungs of neonatal Mig-6-/- mice display severe morphological defects, such as airway over-branching and abnormal vascularisation, as well as increased EGF signalling and altered cell proliferation and apoptosis. Correspondingly, in a human lung epithelial cell line, MIG-6knockdown increases EGF signalling, as well as cell proliferation, whereas it promotes apoptosis in a lung endothelial cell line. Interestingly, surviving adult Mig-6-/- mice develop features that resemble obstructive pulmonary disease, which does not occur when Mig-6 is conditionally inactivated in adult mice. These data support an important,partly EGF-mediated, role for Mig-6 in lung development, and future studies should address the significance of MIG-6 for human lung disease.