XIAP and acute pancreatitis: In summary, our study demonstrates that XIAP is a key mediator of cell death in acute pancreatitis through its effects on caspases, RIP1 and NF-κB. Lack of XIAP in acute pancreatitis decreases the activation of NF-κB, increases caspases activities and RIP1 degradation, leading to less inflammatory response, increased apoptosis and decreased necrosis in acute pancreatitis, resulting in reduced severity of acute pancreatitis.