This paper attempts to demonstrate the influence of gallstones, from different locations, on ultrastructural changes in pancreatic acinar cells. Forty-two gallstone patients with no record of clinical pancreatitis are the subjects of this study. Of these patients, 14 have cholecystolithiasis, 14 have choledocholithiasis, and 14 have primary hepatolithiasis. The findings reveal the following ultrastructural alterations of the pancreatic acinar cells: dilation of the rough endoplasmic reticulum, accumulation of lipid droplets, an increase of auto-phagic vacuoles, residual bodies and myelin figures, alteration of electron density of zymogen granules, and alteration of mitochondria. All these ultrastructural changes are similar to those of clinical acute pancreatitis. With three locations of calculi, these different kinds of gallstones have a similar affect on the fine structure of pancreatic acinar cells, and these changes occur regardless of the size of the common bile duct and the biochemical data. This suggests that irrespective of the location of the gallstones, subclinical cellular injury to acinar cells is caused.