IFNA1 and chronic granulomatous disease: In 2014, Kelkka and colleagues reported that both chronic granulomatous disease (CGD) patients and mice lacking functional NOX2 complex exhibit a prominent type I interferon (IFN) response signature and elevated levels of autoantibodies [25], suggesting for the first time that type I IFN signaling as a potential mediator connecting ROS deficiency to autoimmunity.