Mechanistically, YTHDF2 alleviated the inflammatory response in sepsis by directly recognizing and binding to the m6A-modified site in the IL-6R 3′-UTR to accelerate the degradation of IL-6R mRNA, which consequently blocked the activation of the JAK2/STAT1 pathway and finally reduced the release of HMGB1 (Figure 6). This evidence concerns the gene STAT1 and Sepsis.