Previous studies have established that intrapancreatic trypsinogen activation mediated by Cathepsin‐B (CTSB), leads to autodigestion and promotes pancreatic damage.[19] P62‐driven autophagy‐dependent ferroptosis,[20] Complement activation‐induced acinar cell damage [21, 22, 23, 24] and the recruitment of immune cells through cytokines IL‐1B, TNF, and adhesion molecule ICAM1[25, 26, 27] have been reported as crucial mechanisms in pancreatitis. The gene discussed is TNF; the disease is pancreatitis.