Aberrant pancreatic enzyme activation triggers NF-κB-mediated inflammatory cascades, leading to the sequential release of pro- and anti-inflammatory mediators (e.g., IL-6, IL-8, MCP-1; HGF, and sTNF-αR1) with severe cases show an early pro-inflammatory surge, while anti-inflammatory mediators dominate later stages.38,39 This heterogeneity in inflammatory phenotypes affects immune cell infiltration in the pancreas and is closely associated with organ failure and complications, thus accurate identification of inflammatory status is crucial for personalized treatment of AP. Here, CCL2 is linked to alkaline phosphatase measurement.