In addition, exposure of mitochondrial DNA can also activate TBK1 and increase the expression of IFN-I through cGAS and STING; YAP can directly hinder IRF3 dimerization and nuclear translocation, as well as inhibit TBK1 K63 ubiquitination, and block its interaction with MAVS, STING and IRF3, reducing the expression of IFN-I; but IKK activation in response to viral infection can also cause the degradation of YAP; and MST1-mediated IRAK1 (negative regulatory molecule of RIG I and TRIF) degradation increases the activation of IRF3 and the production of IFN-I. Here, TBK1 is linked to viral infectious disease.