In patients with SLE, accelerated neutrophil death and the deficiency in clearing dying neutrophils cause nuclear and cytoplasmic antigen exposure, excessive production of type I interferon (IFN), and neutrophil extracellular trap (NET) release, subsequently inducing autoimmune responses (Garcia-Romo et al., 2011). Here, IFNA1 is linked to systemic lupus erythematosus.