Since it has been previously shown that microglial NADPH oxidase can be stimulated by interleukin-1β to produce hydrogen peroxide35, it is possible to hypothesize that during experimental multiple sclerosis, persistent inflammation and microglial activation may trigger an increase of interleukin-1β levels, NADPH oxidase over-expression and subsequent loss of neuroplasticity. The gene discussed is FMO5; the disease is multiple sclerosis.