New research has helped unravel a link between mitochondria, neutrophil extracellular traps (NETs), and inflammation in autoimmune disorders. Lood et al. found that mitochondrial reactive oxygen species (ROS) could stimulate NETosis after mitochondrial activation by ribonucleoprotein immune complexes. Immune complex stimulation precipitated a release of oxidized mtDNA, which triggered interferon signalling and an immune response. This response could be ameliorated through inhibition of ROS production. ROS was also required for NETosis of low-density granulocytes found in patients with systemic lupus erythematosus.