This hypothesis is based on previous evidence showing that: (a) C5a/C5aR1 signaling directly triggered neutrophil activation (e.g., granule enzyme release and superoxide anion production/respiratory burst) in several pathological conditions (66–71); (b) C5aR1 signaling induced neutrophils to degranulate — with increase in CD66 expression — in sepsis models (72); (c) C5a levels in the soluble fraction of sputum correlated positively with markers associated with worse cystic fibrosis lung disease, including NE levels, MPO activity, and DNA concentration (73). The gene discussed is C5AR1; the disease is Sepsis.