Diabetes and its complications represent one of the major threats to public health worldwide. Increasing evidence in human and animal models indicates that deficient β-cell function is an essential factor for the development of the disease. Genetic studies have led to the identification of numerous susceptibility genes for type 2 diabetes, most of which regulate β-cell glucose metabolism, gene expression, or insulin secretion. The need to elucidate further the physiology of β cells in normal and pathologic conditions and alleviate the burden of diabetes could not be more compelling.