Mice invalidated for Gjd2 feature alterations in beta cell function which are reminiscent of those that precede the development of overt diabetes in humans (e.g., loss of insulin oscillations) and, later, characterize the disease (e.g., increased basal release of insulin and failure to increase the insulin output in the presence of postprandial concentrations of glucose) [51, 62, 235, 248, 252, 256]. Here, GJD2 is linked to diabetes mellitus.