Hu et al. have also shown that viral infection promotes an increase in intracellular BAs, resulting in activation of Src kinase through the TGR5-GRK-β-arrestin axis, that modulates tyrosine phosphorylation of various antiviral signaling components such as retinoic acid-inducible gene I (RIG-I), virus-induced signaling adaptor (VISA), mediator of IFN regulatory transcription factor 3 activation (MITA), TANK binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3) in order to enable the innate antiviral immunity [51]. The gene discussed is IRF3; the disease is viral infectious disease.