STING1 and viral infectious disease: Phosphorylated PKR can block translation initiation via phosphorylating eIF2 on Ser51 to induce cell death,76 and activate NFκB via phosphorylating IKKB to induce innate immune.77 Another group of non-RLR RNA helicases could also sense RNA and mediate inflammasome, or enhance RLR signaling to enhance IFN response and virus infection inhibition effect.78 One study reported that, upon binding to dsDNA, the NOD-like receptor family CARD domain containing 3 (NLRC3) could unleash STING from its sequestration, which induces STING mediated immunity activation.79