Although the detailed mechanisms remain unclear, the CTT of STING and its ER to Golgi translocation have been shown to be indispensable for inducing NF-κB signalling.28,29 While TBK1 activity has been reported to magnify NF-κB responses, it seems to be not essential for NF-κB activation.28,30 Moreover, signal transducer and activator of transcription 6 (STAT6) was reported to be recruited by STING for TBK1-mediated phosphorylation during viral infection. Here, NFKB1 is linked to viral infectious disease.