A major surge of interest has recently focused upon nitric oxide (NO) as a mediator of autoimmune destruction ofβ-cells in insulin-dependent diabetes mcllitus (IDDM). It has been proposed that insulin producing cells in response to cytokines are induced to produce self destructing amounts of NO, and that endothelial cells or islet infiltrating macrophages may induceβ-cell death by releasing cytotoxic levels of NO within the islet. Recent findings in this field are presently discussed and we conclude that although NO might have a role in rodent IDDM, any putative role of NO in the pathogenesis of human IDDM remains to be clarified.