Although TRIM28 can be phosphorylated in response to viral RNA in a PKR-dependent manner (21), infection-induced loss of posttranslationally modified TRIM28 was independent of all canonical antiviral RNA-sensing mechanisms, as IAV triggered this response even in the absence of RIG-I, MDA5, PKR, or MAVS (SI Appendix, Fig. S1 A and B), and IFN-α treatment alone failed to trigger this phenotype (Fig. 2E). Here, MAVS is linked to infection.