In cerulein‐induced pancreatitis models, ferroptosis plays a crucial role in its pathogenesis.[20, 37] CTSB activates trypsinogen in acinar cells, causing acinar cell death, followed by a pro‐inflammatory response and leukocyte migration, exacerbating local injury and increasing the severity of pancreatitis.[19] Strikingly, the transcriptomes of pancreatic from mice infected with SFTSV and from mice treated with cerulein both highlight the central role of complement hyperactivation‐inflammation cascades in pancreatitis. The gene discussed is CTSB; the disease is pancreatitis.