We found that phosphorylation of TBK1 in TRIM18 KO BMDM was significantly enhanced relative to that in WT BMDM after infection with CVB3 or adenovirus (Fig. 6g), suggesting that TRIM18 indeed recruited PPM1A to dephosphorylate TBK1 for TBK1 inactivation. Here, PPM1A is linked to infection.