Although the exact mechanisms are for the most part unknown, there is some evidence that the severity and outcome of AP might be determined by the acinar cell response to activation of trypsinogen, as well as the events that occur subsequent to acinar cell injury, including activation of transcription factors such as nuclear factor-kappa B (NF-κB), recruitment of inflammatory cells, and generation of inflammatory mediators [1], [5]. This evidence concerns the gene NFKB1 and alkaline phosphatase measurement.