Upon viral infection, MITA undergoes phosphorylation, ubiquitination, and subcellular translocation to subsequently function as an adaptor protein that recruits TANK-binding kinase 1 (TBK1) and IRF3 to the mitochondrial antiviral signaling protein (MAVS)-associated complex, thereby facilitating the activation of IRF3 [22]. Here, MAVS is linked to viral infectious disease.