Bergin et al found that in clinically stable ZZ patients, the neutrophils have increased levels of TACE activity on their membranes, leading to a higher chemotactic index.90 Post AAT augmentation therapy, the increase in plasma concentration of AAT resulted in normalized ZZ-AATD neutrophil chemotactic responses by inhibiting TACE activity and thereby preventing FcγRIIIB from being shed from the cell membrane, reducing it to that of healthy control levels. This evidence concerns the gene ADAM17 and alpha 1-antitrypsin deficiency.