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Douglas B. Kuhns, Ph.D., W. Gregory Alvord, Ph.D., Theo Heller, M.B., Ch.B., Jordan J. Feld, M.D., M.P.H., Kristen M. Pike, M.S., Beatriz E. Marciano, M.D., Gulbu Uzel, M.D., Suk Find DeRavin, M.D., Ph.D., Debra A. Long Priel, M.S., Benjamin P. Soule, M.D., Kol A. Zarember, Ph.D., Harry L. Malech, M.D., Steven M. Holland, M.D., and John I. Gallin, M.D.: Residual NADPH Oxidase and Survival in Chronic Granulomatous Disease Chronic granulomatous disease, initial described in the 1950s,1 is a rare genetic disease without ethnic preference. The risk of death among individuals with persistent granulomatous disease is 1 to 5 percent each year, and the extent of risk provides been thought to depend on whether inheritance is an autosomal recessive trait or an X-linked trait.2 Chronic granulomatous disease is caused by defects in any among five subunits of phagocyte-derived NADPH oxidase, including gp91phox , p22phox , p47phox , p67phox , and p40phox 3; in rare circumstances there is an association with glucose-6-phosphate dehydrogenase.4 In patients with chronic granulomatous disease, the creation of superoxide anion and other reactive oxygen intermediates by neutrophils, monocytes, macrophages, and eosinophils is impaired, resulting in recurrent infections, granulomatous problems, and premature death.