STING1 and Sepsis: As shown in Figure 7A–D, the levels of STING, p‐TBK1, and p‐IRF3 in the hippocampus of mice in the CLP group were significantly greater than those in the Sham group indicating that the STING‐TBK‐IRF3 pathway in the hippocampus was activated during sepsis, which can further trigger neuroinflammation.