A wealth of data in animal models indicates that type 1A diabetes results from T cell-mediated specific destruction of islet β cells. There is evidence for the NOD mouse model that insulin is the primary autoantigen and a specific insulin peptide B:9-23 is central to pathogenesis. It is also now possible to predict the development of type 1A (immune mediated) diabetes for the great majority of individuals with a combination of genetic, immunological and metabolic parameters. Such prediction is possible because of the chronic nature of the autoimmunity and loss of β cell function that precedes the disease. Given the ability to predict type 1A diabetes trials at all stages of the disorder to prevent β cell destruction are now possible.