DURING the past decade a wealth of information concerning the pathogenesis of Type I diabetes has become available. Two spontaneous animal models of the disease have been discovered and characterized (the Biobreeding rat and the non-obese diabetic mouse); the importance of a gene or genes in the major histocompatibility complex in Type I diabetes of human beings, of mice, and of rats has been appreciated; and the prognostic importance of selected assays for islet-cell antibodies has been defined. T-cell abnormalities that precede diabetes have been discovered. Evidence has suggested that progressive loss of first-phase insulin secretion precedes diabetes, and immunologic . . .