The early findings of certain enhancements of neutrophil function led to a clinical trial of IFN-γ in patients with CGD, a group of genetic disorders characterized by defects in components of the NADPH oxidase [6], a multiprotein, transmembrane complex that generates large quantities of superoxide anion (O2-) in response to specific agonists or phagocytosis (the oxidative burst). This evidence concerns the gene FMO5 and chronic granulomatous disease.