In contrast, Qin et al. have delineated that RNF26, mainly located at ER and constitutively interacting with STING, promotes the K11-linked polyubiquitination of STING at lys150, which modification unlocks the virus-triggered K48-linked poly-ubiquitination of STING to prevent its proteasomal degradation.262 This regulatory mechanism is required for rapid and efficient induction of both IFN-I and proinflammatory cytokines at an early stage of viral infection. The gene discussed is STING1; the disease is viral infectious disease.