RIP1, a key regulator of programmed necrosis in many diseases including acute pancreatitis, has been known to be cleaved/inactivated by caspase-3 and -8,23, 27 and also regulated by XIAP.28, 29 Previous studies showed that enhanced protein levels of XIAP resulted in increased RIP1 production as well as decreased degradation, while genetic inhibition of XIAP expression markedly increased RIP1 degradation/inactivation in the pancreatic acinar cells.48 Our studies indicate that deletion of XIAP promotes the degradation/inactivation of RIP1 in cerulein+LPS-induced pancreatitis. The gene discussed is XIAP; the disease is acute pancreatitis.