It is commonly accepted that type 1 diabetes (T1D) is an autoimmune and inflammatory disease that results from the wholesale yet surprisingly selective killing of the insulin-secreting β-cells of pancreatic islets. While the relative importance of reduced β-cell function versus reduced β-cell mass is currently debated in type 2 diabetes, T1D has been considered the classic example where diabetes results from reduced β-cell mass secondary to autoimmune attack. However, this view has recently been challenged.