It has been known for decades that some people with apparent type 2 diabetes have evidence of islet autoantibod-ies associated with p-cell autoimmunity (1). This population is highly heterogeneous, with varying prevalence and overlapping clinical, biomarker, and genetic features between type 1 diabetes and type 2 diabetes (2). The extent to which this represents an intermediate phenotype of autoimmune diabetes, or a mixture of autoimmune and nonautoimmune diabetes as a result of an interaction between imperfect assay specificity and low prevalence of type 1 (autoimmune) diabetes in this population, is a matter of debate (2, 3).
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