GM-CSF is induced by the presence of airway pathogens30, 31 and is known to be an important regulator of the activation and survival of key effector cells in COPD, namely the neutrophil and macrophage.32, 33 Critically, neutralisation of GM-CSF in animal models attenuates airway inflammation in response to cigarette smoking.7 However, to date there has been a paucity of direct evidence of increased GM-CSF expression in airway secretions. Here, CSF2 is linked to chronic obstructive pulmonary disease.