IFNA1 and infection: 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).