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). The gene discussed is TNF; the disease is acute respiratory distress syndrome.