Since β-catenin has been reported to promote the maintenance and proliferation of mature acinar cells under normal and AP conditions (Keefe et al., 2012), and reduce the severity of AP by decreasing pancreatic acinar cells necrosis in, and inflammatory factors release from, pancreatic acinar cells (Huang et al., 2019), while NF-κB is known to play key roles in the pathogenesis and progression of AP (Rakonczay et al., 2008; Jakkampudi et al., 2016), and activation of NF-κB in the pancreas can induce an inflammatory response in pancreatic acinar cells (Chen et al., 2002). This evidence concerns the gene NFKB1 and alkaline phosphatase measurement.