GAST encodes gastrin, a hormone produced by G-cells in the stomach and duodenum that plays dual roles in gastrointestinal regulation and systemic sodium homeostasis. Gastrin stimulates gastric acid secretion and pancreatic enzyme release while promoting smooth muscle contraction and increasing blood circulation and water secretion in the stomach and intestine. Beyond its classical digestive functions, gastrin acts as an enterokine through the cholecystokinin B receptor (CCKBR) to regulate renal sodium excretion following oral sodium intake 1. This gastrorenal axis function is critical for blood pressure regulation; germline deletion of GAST or CCKBR in mice causes salt-sensitive hypertension, and selective gastrin silencing impairs sodium excretion and increases blood pressure 1. In disease contexts, GAST variants are associated with peptic ulcer disease susceptibility, likely through effects on gastric acid secretion and infection-related damage response 2. The chr17 loci of GAST are linked to human essential hypertension 1, suggesting genetic variation in this gene may contribute to blood pressure dysregulation in humans. These findings indicate GAST functions not only in acute digestive responses but also in chr17 regulation of cardiovascular homeostasis through sodium handling.