Yet, PR3 is a promising drug target for COPD and CF for several reasons: higher levels of PR3 than hNE are released from neutrophil azurophil granules, PR3 is active as both a membrane-bound and a free enzyme, PR3 is present in a larger area of the cell than hNE and local lung derived inhibitors have less impact on PR3 than hNE [16–18]. This evidence concerns the gene PRTN3 and cystic fibrosis.