The damage of the exocrine cells in type I diabetes is most likely multifactorial, with a number of possible causes: (a) the lack of the trophic action of insulin (and possibly of glucagon and somatostatin) on acinar cells; (b) an involvement of the exocrine tissue in the autoimmune destruction of islet cells; (c) autonomic diabetic neuropathy leading to enteropancreatic reflex impairment; (d) hypoxic sufferance of exocrine tissue due to microvascular damage [26, 27]. This evidence concerns the gene INS and type 1 diabetes mellitus.