Twenty two of sixty-seven examined SLE patients had evidence of polymerization of the mitochondrial antiviral signaling protein MAVS, which is downstream of both RIG-I and MDA5 (Figure 1B) and acts by generating a protein complex that activates the kinases required for IRF3 activation and type I IFN production. The gene discussed is MAVS; the disease is systemic lupus erythematosus.