The original report by Stabile et al1 that the gastrinoma triangle harbored most sporadic gastrinomas was a seminal clinical observation. Its importance to the study of gastrointestinal endocrine tumors is no less than that of William Beaumont to gastric physiology. From the observation that most sporadic (nonhereditary, ie, multiple endocrine neoplasia type I) gastrinomas occurred in the gastrinoma triangle, these investigators have continued to examine this phenomenon. They have removed the mystery from the "ectopic" gastrinomas. The mystery sprung from the false concept that all gastrinomas should arise in the pancreas; the original patients had pancreatic neoplasms. No gastrin-containing cells can be identified in the adult human pancreas. The authors' work has been hampered by the relative rarity of these tumors and the inability to conduct a prospective randomized trial. However, their prescient observation and persistent examination have led them to their current description.2 Passaro et al2 provide a strong argument for 2 types of sporadic gastrinomas: those that occur (most) in the gastrinoma triangle that apparently arise from a stem cell from the ventral pancreatic bud, the cells of which produce pancreatic polypeptide—a marker of ventral bud origin—and those that arise outside. Tumors that arise in the gastrinoma triangle or, possibly, from the ventral bud have different, less aggressive, biologic behavior from those sporadic gastrinomas that arise outside the triangle. The authors propose that the role of these cells during early fetal development (none can be found in the adult) may possibly be related to the known trophic effects of gastrin, which we and others have described, and that they are vital for the development of the gut; this may explain the less aggressive tumors.