In recent years, multiple proteins have been identified to control RLR signal transduction, thereby maintaining the balance of physiological functions; for example, GSK3β interacts with TBK1, resulting in TBK1 phosphorylation at Ser172 and facilitating TBK1 activation after viral infection (31), and SHIP-1 (inositol 5′-phosphatase) targets TBK1 to negatively regulate TLR3- or TLR4-induced IFN-β production (32). The gene discussed is TLR3; the disease is viral infectious disease.