During the five decades after Hashimoto described struma lymphomatosa of the thyroid gland featuring diffuse lymphocytic infiltration, fibrosis, and parenchymal atrophy,¹ autoimmunity became increasingly recognised, such that when similar histological changes were described affecting the pancreas, an autoimmune mechanism was postulated.² Autoimmune pancreatitis then remained among a number of plausible explanations for the appreciable minority of patients with chronic pancreatitis who give no history of alcohol abuse.³ More recently, Japanese workers again took up the baton, describing series of patients who had undergone pancreatic resection for suspected neoplasia but whose histology demonstrated lymphocytic infiltration of the exocrine parenchyma, with periductular and interlobular fibrosis.^4,5 Further study demonstrated a T cell predominance to the infiltrate,⁵ autoantibodies directed against carbonic anhydrase II,⁶ an enzyme present in pancreatic as well as salivary ductal epithelium, and frequently high serum levels of IgG4.⁷ These findings have been confirmed in the European population, as reported by Aparisi et al in this issue of Gut,⁸ who describe a small series within a larger group of patients with non-alcoholic chronic pancreatitis (see page 703). Although not stated, such a group is highly likely to include patients with mutations of the cystic fibrosis transmembrane conductance regulator (CFTR)⁹ and serine protease inhibitor Kazal type 1 (SPINK1)¹⁰ which both increase the risk of chronic pancreatitis, as well as mutations of cationic trypsinogen (protease, serine, 1 (trypsin 1): PRSS1) which cause hereditary …