Latent autoimmune diabetes in adults (LADA) is the most prevalent form of adult-onset autoimmune diabetes and probably the most prevalent form of autoimmune diabetes in general. It shares clinical and metabolic features with both type 2 diabetes mellitus (T2DM) and type 1 diabetes mellitus (T1DM). Patients with LADA may initially be diagnosed incorrectly as having T2DM based on their age, particularly if they have risk factors for T2DM such as a strong family history or obesity. The diagnosis of LADA is typically based on the finding of hyperglycemia together with the clinical impression that β-cell failure rather than insulin resistance (IR) is the main cause; detection of a low C-peptide and raised antibodies against the islets of Langerhans support the diagnosis. Highly variable β-cell destruction, different degrees of IR and heterogeneous titer and pattern of islet autoantibody, suggesting different pathophysiological pathways partially explaining the heterogeneous phenotypes of LADA. The decline in β-cell function progresses much faster in LADA than in T2DM, presumably because of the ongoing autoimmune assault in LADA, and therefore necessitates insulin therapy much earlier in LADA than in T2DM. The existence of heterogeneous phenotypes in LADA makes it difficult to establish an a priori treatment algorithm, and therefore, an individualized pharmaceutical therapy is required to preserve residual β-cell function and attain optimal diabetic control to decrease the risk of long-term diabetic complications in patients with LADA. This article aims to give an overview of the current understanding and gaps in knowledge regarding epidemiology, clinical and metabolic features, genetics, immunology, complications and therapeutic strategy of LADA and summarize an update on results from recent studies on the treatment of the disease.