Intestinal CCKBR can be stimulated by gastrin, which is secreted by antral G cells in the stomach.[16, 17] In animal models of diabetes, improved glucose control and neogenesis of functional β‐cell mass occur after gastrin treatment.[18, 19, 20, 21, 22, 23] Gastrin, via CCKBR, significantly reduced glucose absorption in human intestinal epithelial cells (HIECs) (based on our preliminary exploratory study). The gene discussed is GAST; the disease is diabetes mellitus.