A wealth of data in animal models indicates that type 1A diabetes results from T cell-mediated specific destruction of islet beta 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 beta cell function that precedes the disease. Given the ability to predict type 1A diabetes trials at all stages of the disorder to prevent beta cell destruction are now possible.