This secondary role of AAT is independent of its anti-proteinase activity, as it occurs with both oxidised and heat-inactivated protein.34 This may important in the management of AATD, as it suggests that targeting the neutrophil elastase inhibitory function independently of AAT (for instance with chemical elastase inhibitors) may only partly restore normal homeostasis in the AATD lung, as the effect of AAT on other cell functions may be an important component for the development and treatment of lung disease. Here, SERPINA1 is linked to alpha 1-antitrypsin deficiency.