Neutrophils from AATD patients, incubated under hypoxia for 4 h and stimulated with TNF-alpha and fMLP, showed significantly increased release of active NE (azurophil granules; p = 0.035) (Figure 1A), MPO (azurophil granules; p = 0.042) (Figure 1B), lactoferrin (specific granules; p = 0.015) (Figure 1C), and MMP-9 (gelatinase granules; p = 0.001) (Figure 1D) compared to control individuals (MM). The gene discussed is FPR1; the disease is alpha 1-antitrypsin deficiency.