The reason might be that (1) lnc‐ITSN1‐2 might mediate miR‐125a to activate CD4+ T cell, induce Th17 cell differentiation, and then release the pro‐inflammatory cytokines18; therefore, lnc‐ITSN1‐2 correlated with elevated Th17 cells and inflammation; (2) miR‐125a is a well‐known anti‐inflammatory factor, which inhibits inflammation by regulating the Wnt/β‐catenin and NF‐κB pathways27; thus, lnc‐ITSN1‐2 might target miR‐125a (mentioned above) to promote inflammation, thus causing multiple organ injury, which indirectly increased disease severity in sepsis patients. This evidence concerns the gene NFKB1 and Sepsis.