Although it is known that MAVS contains binding sites for several TRAF proteins (Seth et al., 2005; Xu et al., 2005), the role of these TRAF proteins in MAVS signaling has been enigmatic because cells lacking an individual TRAF protein, including TRAF2, TRAF3, TRAF5, and TRAF6, could still induce IFNβ normally in response to virus infection (Seth et al., 2005; Konno et al., 2009; Zeng et al., 2009). The gene discussed is MAVS; the disease is viral infectious disease.