It is likely that neutrophils are major contributors of properdin in inflammatory microenvironments, because they are the first cells recruited to sites of infection where they facilitate the clearance of microorganisms via phagocytosis, the release of cytotoxic molecules from secondary granules, and the formation of neutrophil extracellular traps (NETs) (reviewed in (30, 31)). The gene discussed is CFP; the disease is infection.