STING1 and viral infectious disease: In this context, STING can directly recruit phosphorylated TBK1, which then activates IRF3 that can directly trigger apoptosis in a BAX–BAK-dependent manner [97,98]; thus, the cGAS–STING pathway-induced activation of IRF3 results in apoptosis rather than a type-I IFN signaling cascade under viral infection or irreversible damage.