Although our in vivo data do not strongly support whether attenuated cellular death in RIG-I-knockdown animals is mediated directly via type 1 interferon response and/or indirectly via host cytokine response upon infection, our results provide one clear explanation as to how transient silencing of RIG-I in motor neuron NSC34 cells attenuated apoptosis by suppressing pIRF3/7 signaling effectively by blocking p-IRF3-induced IFN-independent genes (likely ISG54 and ISG56) and not any other IFN-dependent pathways (interferon-β production and IFNAR signaling). The gene discussed is IFIT2; the disease is infection.