IRF3 and viral infectious disease: The authors reported that in vitro or in vivo deficiency in lncRNA ACOD1 significantly reduced viral load in macrophages and in immune organs through an IRF3/IFN‐I‐independent pathway, and the lncRNA ACOD1 directly interacts with glutamic‐oxaloacetic transaminase 2 (GOT2), which is involved in amino acid metabolism and tricarboxylic acid (TCA) cycles during viral infection (Wang et al., 2017).