However, in about 20% of patients, the inflammatory process involves more than the pancreas, leading to a severe course; almost one-third of these patients progress to systemic inflammatory response syndrome, and, subsequently, develop multi-organ CS1 dysfunction syndrome, which is the main cause of death in critically ill patients. Therefore, preventing SIRS/MODS is crucial in the treatment of patients with AP. Nevertheless, the specific mechanisms underlying the transition from local pancreatic inflammation to SIRS have not yet been elucidated clearly. Individual differences in the occurrence, transition, and development of AP indicates that genetic background may play an important role in AP. The pancreatic protease/anti-protease system and inflammatory cytokines play pivotal roles in the pathogenesis of AP ; hence, most previous studies have mainly focused on polymorphisms occurring in genes related to these systems. It has been reported that the anti-inflammatory response also plays an important role in AP, but limited studies have investigated the relationship between polymorphisms in genes encoding anti-inflammatory molecules and AP. A20, also known as the TNF-a-induced protein 3, is a zinc finger protein that was first identified from a gene, TNFAIP3, that was induced by TNF-a in human umbilical vein endothelial cells ; it is now known that A20 is widely expressed in a variety of human cells. As a dual ubiquitin-editing enzyme, A20 plays a central and ubiquitous role in negatively regulating the activity of the transcription factor NF-kB and the proinflammatory gene expression that is triggered by signaling from Toll-like receptors and NOD2. The inhibitory KPT330 Selinexor effect is mediated by inactivation of several proteins that are critical to NF-kB signaling, such as RIP1/2, TRAF2/6, NEMO, and TAK1, through ubiquitination or de-ubiquitination. A20 plays a critical role in the pathogenesis of inflammatory diseases. Factors underlying genetic predisposition for the development and progression of AP are largely unknown.Although several gene variants have been implicated in the susceptibility to and/or progress of AP, the effect of variants in genes involved in negative regulation of inflammation signaling pathways on AP has rarely been reported.