Based on a previous study (19) and our report, clinically relevant arguments to increase AAT augmentation therapy to more physiological levels may be (a) to facilitate an improved inhibition of ECM-degrading NE activity in the bronchoalveolar space of AATD patients (19) and (b) to better protect AATD patients against increased AAT turnover expectedly developing upon lung bacterial infections, which would also lower the risk of emphysema progression/exacerbation. Here, SERPINA1 is linked to alpha 1-antitrypsin deficiency.