CRK and acute pancreatitis: In this model, with the induction of acute pancreatitis, the pancreatic acinar cell group I PAKs (PAK1) were overexpressed, which led to the activation of NF-kB and the p38 signaling cascade, which in turn resulted in the pathological features of acute pancreatitis including serum concentrations of amylase and lipase and increased levels of tissue necrosis factor alpha, interleukin-6 and interleukin beta.