Conversely, a lack of ROS has been shown to enhance azurophil granule exocytosis in response to TNF-α and fMLP, as pharmacological inhibition of NADPH oxidase (which is responsible for ROS generation) enhanced NE release, an effect recapitulated using neutrophils from patients with chronic granulomatous disease (CGD) who have a defective NADPH oxidase complex [90]. The gene discussed is FPR1; the disease is chronic granulomatous disease.