“…An important recent advance in pancreatitis genetics was the discovery of TRPV6 (encoding transient receptor potential cation channel subfamily V member 6; MIM# 606680) as a new CP susceptibility gene (Masamune et al, 2020; Sahin‐Tóth, 2020; Zou et al, 2020). Compared with other developments in the field of pancreatitis genetics over the last 10 years, which were either limited to specific populations or involved a small genetic effect (Burgos et al, 2021; Fjeld et al, 2015; Lasher et al, 2019; Moore et al, 2019; Rosendahl et al, 2018; Tang et al, 2018; Whitcomb et al, 2012; Witt et al, 2013; Wu et al, 2017; Zou et al, 2016), the TRPV6 discovery was noteworthy in that aggregated functionally deficient TRPV6 variants were found to exert a very strong genetic effect on CP across four populations; indeed, the corresponding odds ratios (OR) were 8.9 in the Chinese cohort (Zou et al, 2020), 48.3 in the Japanese cohort, and infinity in the French and German cohorts (Masamune et al, 2020). Unlike most other CP genes, TRPV6 is expressed in several types of epithelial cells, including pancreatic ductal and acinar cells, and encodes a constitutively active Ca 2+ ‐selective ion channel (Fecher‐Trost et al, 2017; Stoerger & Flockerzi, 2014).…”