Diabetes mellitus in humans is a heterogeneous disorder classified clinically into two main types. The diagnosis of type 1 versus type 2 diabetes is made phenotypically using criteria such as age at onset, abruptness of hyperglycemic symptoms, presence of ketosis, degree of obesity and the perceived need for insulin replacement. The pathogeneses of type 1 and type 2 diabetes are believed to be different. Type 1 diabetes is an autoimmune disease mediated by cellular effector mechanisms; whereas classic type 2 diabetes is not autoimmune but results from insulin resistance and a nonautoimmune insulin secretory defect. Most type 1 diabetes patients are diagnosed in childhood or young adulthood before the age of 35 years. However, there is clearly a subgroup of patients clinically diagnosed with type 2 diabetes who are greater than 35 years of age and have evidence of autoimmunity. The disease of these autoantibody-positive type 2 diabetics is often termed latent autoimmune diabetes in adults (LADA), slowly progressive type 1 diabetes, latent type 1 diabetes, and type 1.5 diabetes. This group of patients comprises approximately 10-15% of Caucasian type 2 diabetes patients. Type 1.5 diabetes patients tend to present with islet cell autoantibodies, islet-reactive T cells, higher HbA(1c) levels, lower C peptide, and a propensity toward insulin dependency compared to autoantibody-negative classic type 2 diabetes subjects.