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h 2 Patients with hereditary pancreatitis due to a serine protease (PRSS1) gene mutation are well known to develop pancreatic xocrine insufficiency and diabetes in later life, and represent a igh-risk group for pancreatic cancer (PC) [1] . In contrast, the natral history of acute recurrent or chronic pancreatitis (CP) paients with serine protease inhibitor Kazal type 1 (SPINK1) mutaions remains controversial. The c.101A > G (p.N34S) mutation is the ost common, present even in 1–2% of otherwise healthy individals. Although an underlying molecular mechanism has yet to be dentified, this variant is thought to be a disease-modifying factor hat lowers the activation threshold of trypsin. The next most freuent mutation is the c.194 + 2T > C mutation, which has often been eported in East-Asian populations [2] . In the c.194 + 2T > C varint, because exon 3 encoding the trypsin-binding site is skipped ue to a slicing aberration, trypsin activation cannot be inhibited, nd continuous inflammation leads to CP [3] . Several reports have hown that both variants are related to increased risk of CP [ 4 , 5 ], ut a meta-analysis revealed a lower association between SPINK1 ariants and development of PC [6] . In an article in EBioMedicine, Muller and colleagues retrospecively reviewed 209 patients with SPINK1 mutations and 302 paients with idiopathic pancreatitis as controls [7] . Importantly, the ancer risk was 12-times higher in patients with SPINK1 mutations han in controls. The cumulative rates of PC before 50, 60, 70, and 0 years old were 0.8%, 11.9%, 27.7%, and 51.8%, respectively. In the 50-years-old population, these rates are similar to that in heredtary pancreatitis (HP) patients with or without PRSS1 mutation 8 , 9 ]. Since the p.N34S mutation was observed in 176 of the 209 atients (154 heterozygous patients, 22 homozygous patients), inolvement of other in the development of PC would be expected.

Is SPINK1 gene mutation associated with development of pancreatic cancer? New insight from a large retrospective study