Type 1 diabetes (T1D) is caused by interactions of genetic predisposition, immunologic triggers, and environmental events leading to autoimmune-mediated pancreatic β-cell destruction and insulin deficiency, although some subjects show lack of autoantibodies to pancreatic islets. Regarding the time lag of complete β-cell mass loss in T1D, simple or unique patterns may not be identified, with some individuals progressing for more than several years. Contrary to T1D, type 2 diabetes (T2D), irrelevant of autoimmune-mediated β-cell destruction, is a heterogeneous disorder characterized by insidious onset and insulin resistance with relative insulin secretory dysfunction. Clinically, some diabetic patients exhibit autoimmune antibodies without insulin requirement. This biphasic type of diabetes is a special form of diabetes that is clinically similar to the early stage of T2D and pathophysiologically defined as a disorder of the autoimmune-mediated progressive β-cell dysfunction. To clarify different features from T1D and T2D, Zimmet [1] introduced the eponym "latent autoimmune diabetes of adults" (LADA) to describe this subgroup of adult phenotypic T2D patients positive for autoantibodies. Based on the natural history of LADA, in which secretory β-cell dysfunction is prominently aggravated depending on the presence of antibodies seen in T1D, Stenstrom et al. [2] suggested LADA is not always a latent disease. Therefore, autoimmune diabetes in adults with slowly progressive β-cell failure might be a more adequate concept. The Immunology of Diabetes Society (IDS) has proposed criteria to standardize the definition of LADA: 1) ≥35 years of age, 2) positive for at least 1 of the 4 antibodies commonly seen in T1D patients; islet cell autoantibodies (ICA), anti-glutamic acid decarboxylase (anti-GAD), Insulinoma-associated protein-2 antibodies (IA-2A), and insulin autoantibodies (IAA), and 3) not requiring insulin therapy within the first 6 months after diagnosis [3].