Starting with the observation that FAK deficiency enhances RNA virus replication and impairs NF-κB and IFN-β signaling, Bozym et al. demonstrated that, in response to virus infection, FAK is recruited to the mitochondrial membrane, where interacts with MAVS to enhance NF-kB- and IFN-β-mediated antiviral signaling (Figure 2a) [56]. The gene discussed is IFNB1; the disease is viral infectious disease.