The maximal reduction in the proteinase footprint above 10 μM observed from the fibrinogen buffer model with AAT alone in the presence of activated neutrophils was supportive of the targeted treatment threshold of 11 μM for AAT augmentation therapy to provide maximum protection for local connective tissue from excess degradation in AATD (The Alpha-1-Antitrypsin Deficiency Registry Study Group, 1998). The gene discussed is SERPINA1; the disease is alpha 1-antitrypsin deficiency.