Necroptosis or regulated necrosis has potential clinical relevance since Rip3−/− mice are protected from experimental caerulein-induced pancreatitis.38 As a result, it appears plausible that the enhanced expression of RIP3 coupled to the hyperphosphorylation of its substrate MLKL that we observed in human CP specimens reflects a pathophysiologically relevant event of necroptotic signaling. This evidence concerns the gene MLKL and pancreatitis.