Chronic pancreatitis (CP) is initiated by acinar cell necrosis driving subsequent pancreatic fibrogenesis, according to the necrosis–fibrosis hypothesis developed by Kloppel et al.11, 12 Importantly, some forms of necrosis may be regulated and executed by specific proteins.13 One version of regulated necrosis, necroptosis, is executed by a kinase, receptor interacting proteins 3 (Rip3), and its downstream phospho-rylation target mixed lineage kinase domain-like protein (Mlkl). This evidence concerns the gene RIPK3 and chronic pancreatitis.