However, after infection with CVB3 or adenovirus, interaction between TBK1 and MAVS or STING in both WT and TRIM18 KO BMDM was evident, but significantly enhanced in the TRIM18 KO BMDM relative to levels in WT BMDM (Fig. 6h), indicating that the recruitment of PPM1A by TRIM18 blocked interaction between TBK1 and its upstream adaptors MAVS or STING in macrophages after virus infection. This evidence concerns the gene MAVS and viral infectious disease.