CF patients fail to clear bacteria from their airways due to a number of host-defense abnormalities, including proteolytic cleavage of the complement C3b receptor (CR3) from the surface of neutrophils, thereby preventing opsonin-facilitated PA phagocytosis (Tosi et al. 1990), proteolytic destruction of lactoferrin (Rogan et al. 2004), reduced airway production of the anti-bacterial compound, nitric oxide (Downey and Elborn 2000; Kelley and Drumm 1998), and excessive accumulation of extracellular HMGB1 (Chirico et al. 2015; Entezari et al. 2012). This evidence concerns the gene LTF and cystic fibrosis.