Recent studies have pushed the neutrophil, an essential component of the innate immunity, to the forefront of the pathogenesis of SLE.1 Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2), constitutively expressed in neutrophils, plays a pivotal role in producing cytosolic reactive oxygen species (ROS).2 ROS-mediated stress has been implicated in various autoimmune and immunodeficiency diseases, including SLE. Here, CYBB is linked to systemic lupus erythematosus.