Upon binding to viral RNAs, RIG-I undergoes conformational changes that activate MAVS, subsequently triggering the activation of TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3), leading to the production of type I interferons (IFNs) and other antiviral cytokines crucial for limiting viral infection (5, 6). The gene discussed is MAVS; the disease is viral infectious disease.