To examine whether STING activation was initiated by EV-A71 infection directly or indirectly, we inactivated EV-A71 using β-propionolactone.51 We observed that inactivated EV-A71 particles did not trigger STING phosphorylation and downstream innate immune activation when compared to untreated EV-A71 (Supplementary Fig. 1f). This evidence concerns the gene STING1 and infection.