Background: Currently, more than half a billion adults are affected by diabetes globally, and the number is foreseen to rise to nearly 800 million by 2045, with the majority being type 2 diabetes mellitus (T2D). Type 2 diabetes (T2DM) is a complex metabolic disease in which the pathophysiology involves an interaction between genetic predisposition and environmental triggers. Hyperglycemia develops as a result of pancreatic islet failure in lieu of systemic insulin resistance. Islet failure in T2DM is associated with a deficit in β-cell mass and function and increased glucagon secretion. Insulin resistance in T2DM primarily manifests at the level of skeletal muscle, liver, and adipose tissue, and is characterized by impaired insulin-stimulated glucose disposal, failure to suppress hepatic glucose production, and elevated adipose tissue lipolysis and inflammation. Although we have not completely elucidated the pathophysiology of T2DM so far, it is the case that the disease has a major genetic component. Higher concordance rates are found among monozygotic (96%) than dizygotic (DZ) twins in some. In addition to a considerable number of genetic components associated with T2DM, segregation analysis also suggests the polygenic nature of T2DM. The susceptibility loci of T2DM have been discovered by genome-wide association studies (GWAS) since early 2007. Then, numerous GWAS conducted in different countries and ethnic groups have reported linkage signals at the same or different chromosomes with T2DM, and have successfully identified approximately 75 susceptibility loci related to T2DM. Examples of candidate genes are KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), TCF7L2 (transcription factor 7-like 2, the strongest T2D locus identified to date), IRS1 (insulin receptor substrate 1), MTNR1B (melatonin-receptor gene), PPARG2 (peroxisome proliferator-activated receptor gamma 2), IGF2BP2 (insulin-like growth factor two binding protein 2), CDKN2A (cyclin-dependent kinase inhibitor 2A), HHEX (hematopoietically expressed homeobox) and FTO (fat mass and obesity associated) gene. A previous study found that low IL-10 production capacity is also associated with T2DM.