The prospect of lifelong dependency on exogenous insulin injections and potentially debilitating complications has led scientists to relentlessly search for a cure for type 1 diabetes mellitus (T1DM). As this has proven elusive, attempts to intervene in the disease process have proliferated. In this issue of the Archives, Gabbay et al1 publish the results of a trial attempting to preserve insulin secretory capacity in type 1 diabetic patients. Type 1 diabetes mellitus is characterized by the autoimmune destruction of insulin-producing pancreatic β cells, causing an absolute insulin deficiency. This destruction occurs both before and after clinical disease presentation, and the cause for this immunologic attack is thought to be a combination of both genetic and environmental factors. While genetic predisposition is significant, most individuals with a genetic susceptibility will not develop the disease. It is thought that exposure to a second environmental factor, such as a virus, dietary nutrient, or other antigen, results in disease. The presence of an environmental trigger(s) is supported by the fact that while the prevalence of T1DM varies dramatically in different parts of the world, migrating populations take on the prevalence of their new location relatively quickly.2 It is these potential environmental triggers that have been the target of studies to prevent or intervene in the disease process. Furthermore, the incidence of T1DM has been increasing, particularly in those younger than 5 years,3 adding urgency to our intervention attempts.