TBK1 and infection: IRF3 is located in the cytoplasm of non-stimulated cells, and following viral or other pathogen infection it becomes phosphorylated by TANK-binding kinase 1 (TBK1) and IKK kinases, allowing the formation of homodimers that can translocate into the nucleus and activate the synthesis of IFN-β, acting in synergy with NFκB (Yoneyama et al., 2002; Fitzgerald et al., 2003; Hiscott et al., 2003; Seth et al., 2005).