It was found that the TLR4/MyD88/NF-κB signalling pathway was involved in the anti-inflammatory mechanism of ulinastatin-induced sepsis, and this effect could be reversed by the TLR4 agonist LPS, which further confirmed that ulinastatin could reduce the inflammatory response associated with sepsis by inhibiting the expression of the TLR4/MyD88/NF-κB signalling pathway and ultimately play a role in intestinal protection. This evidence concerns the gene NFKB1 and Sepsis.