In pancreatic beta cells, not only insulin exocytosis per se, but translocation of beta granules toward the plasma membrane--an event upstream of exocytosis--are under the control of glucose. However, the molecular basis of this translocation has been poorly understood. Rab27a-mediated translocation of glucose-induced beta granules is reported in this issue of the JCI. Rab27a or its effector molecule may constitute a novel pharmacological target because potentiation of the Rab27a pathway is expected to restore beta cell glucose competency in patients with diabetes mellitus.