In intestinal epithelial cells, Gastrin/CCKBR stimulation prevents high glucose‐stimulated SGLT1 (SLC5A1) and GLUT2 (SLCA2) expressions, via the PI3K/AKT/eIF4B signaling pathway, with facilitatory effects on the secretion of incretins, which could be therapeutic targets for clinical treatment in T2D. The gene discussed is GAST; the disease is type 2 diabetes mellitus.