Our parent project studies the intracellular accumulation and molecular interaction of proinsulin, insulin and the proinsulin processing enzymes PC1/3, PC2 and CPE, which may be dysregulated during the development of the disease and lead to processing errors. Our interest was focused on proinsulin and insulin, as these are the most abundant molecules of the insulin granule, and their role in disease progression has been highlighted in several studies but has not been systematically investigated. However, other molecules inside the insulin granule, such as chromogranins, secretogranins, and islet amyloid polypeptide (IAPP) might undergo similar processing errors. These may contribute to beta cell demise, thereby leading to their recognition by the immune system. Here, we propose to study the expression and accumulation of insulin granule proteins other than insulin and proinsulin. By approaching this from the perspective of the beta cell, we will strive to provide a more comprehensive understanding of the pathogenesis of type 1 diabetes. Ultimately, this work should help to develop novel therapeutic approaches targeting beta cell dysfunction possibly in combination with antigen specific therapies.