The pathogenesis of SAP-ALI/SAP-ARDS involves multiple pathways, including pancreatic elastase-mediated pulmonary damage (Chen et al., 2024), the specific effects of pancreatic enzymes and serum phospholipase A2 (Elder et al., 2012), and the overproduction of oxidative stress factors, macrophage migration inhibitory factor, and cytokines such as Interleukin-6 (IL-6), and Tumor Necrosis Factor-α (TNF-α) (Akbarshahi et al., 2012). This evidence concerns the gene IL6 and acute respiratory distress syndrome.