Ubiquitination of TBK1 seemed an efficient tactic to activate IFN response because the endogenous TBK1 was K63-linked poly-ubiquitinated at 8 h post Sendai virus (SeV) infection (Fig. 1A, top panel) and accompanied with phosphorylation of IRF3 and STAT1, the indications of the IFN production (Fig. 1A, panels 4–5). Here, TBK1 is linked to infection.