Abstract
Over the past two years, there has been a spectacular change in the capacity to identify common genetic variants that contribute to predisposition to complex multifactorial phenotypes such as type 2 diabetes (T2D). The principal advance has been the ability to undertake surveys of genome-wide association in large study samples. Through these and related efforts, similar to 20 common variants are now robustly implicated in T2D susceptibility. Current developments, for example in high-throughput resequencing, should help to provide a more comprehensive view of T2D susceptibility in the near future. Although additional investigation is needed to define the causal variants within these novel T2D-susceptibility regions, to understand disease mechanisms and to effect clinical translation, these findings are already highlighting the predominant contribution of defects in pancreatic beta-cell function to the development of T21D.