During the early injury phase of AP, pancreatic parenchymal cells release DAMPs; proinflammatory cytokines such as IL-6, tumor necrosis factor α (TNF-α), and interleukin-1β (IL-1β); and chemokines, including IL-8 and monocyte chemoattractant protein-1 (MCP-1).267,268 As AP progresses, inflammatory mediators further amplify both local and systemic inflammatory responses by activating signaling pathways such as the NF-κB pathway and recruiting immune cells, including neutrophils and macrophages, which are critical drivers of disease prognosis (Fig. 6). This evidence concerns the gene IL1B and alkaline phosphatase measurement.