We treated wild-type cells and PLA2G16-overexpressing cells with the TBK1 inhibitor GSK8612 after FMDV infection, examined the STAT1 phosphorylation levels at 12 h and 16 h post infection, and found that STAT1 phosphorylation was blocked in both cases (Figure 5c), suggesting that overexpression of PLA2G16 promotes an elevated STAT1 phosphorylation that is dependent on the classical interferon signaling pathway. This evidence concerns the gene TBK1 and infection.