It not only seems likely that this will be similar in AATD COPD patients with bronchiectasis but may even represent a greater inflammatory burden as seen in AATD exacerbations [34] and be amenable (at least in part) to AAT augmentation intravenously [35], by the inhaled route [36] or with more recent oral antiproteinase strategies in development for non-deficient bronchiectasis [37]. This evidence concerns the gene SERPINA1 and alpha 1-antitrypsin deficiency.