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 autoimmune diabetes of (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].