An important function of A-to-I editing catalyzed by ADAR is to prevent recognition of Alu RNAs by dsRNA sensors, RIG-I, TLR3, and MDA5; loss of A-to-I editing of Alu RNAs results in accumulation of Alu dsRNAs, activation of dsRNA sensors and the triggering of downstream inflammatory responses as observed in both viral infection and autoimmune disease (24, 28). The gene discussed is ADAR; the disease is autoimmune disease.