Indeed, the putative “protective threshold” in the lung epithelial lining fluid is significantly lower than the corresponding threshold in the bloodstream, reflecting these distinct biological compartments.13 Together, these factors suggest the possibility that direct delivery of the normal AAT gene to the lung might circumvent one major impediment to successful gene therapy and in so doing provide a therapeutic benefit to patients with AATD. Here, SERPINA1 is linked to alpha 1-antitrypsin deficiency.