As the acinar body is damaged during its own digestion process, it excessively stimulates pancreatic parenchymal inflammation, which implies that the pathogenesis of HLAP-induced neutrophils and macrophages is infiltrated by inflammatory mediators to release inflammatory markers such as IL-6, IL-1β, TNF-α, etc. These factors activate NF-κB and then produce more inflammatory mediators, causing more serious MODS and SIRS [24,25]. The gene discussed is TNF; the disease is systemic inflammatory response syndrome.