MAVS is a critical converging point of the host response to RNA virus infection. By engaging RIG-I or MDA5, MAVS forms a mitochondrial signalosome, dynamically composed of TRAF2/3/6, TRADD, TOM70, UXT-V1 and so on. This signalosome leads to the activation of TBK1 and IKK and then the ultimate induction of type 1 interferon and inflammatory cytokines, thereby establishing the antiviral state. In addition, MAVS also recruits MAPK kinase MKK7 onto the mitochondria via protein-protein interaction. MKK7 subsequently induces the phosphorylation of JNK2 at its threonine-183 and tyrosine-185 positions. Finally, JNK2 initiates cell apoptosis to sacrifice the virus-infected host cell, thereby dampening virus-induced inflammatory injury.