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Letter

Nature Genetics 39, 770–775 (1 June 2007) | doi:10.1038/ng2043

A variant in CDKAL1 influences insulin response and risk of type 2 diabetes

Valgerdur Steinthorsdottir , Gudmar Thorleifsson , Inga Reynisdottir , Rafn Benediktsson , Thorbjorg Jonsdottir , G Bragi Walters , Unnur Styrkarsdottir , Solveig Gretarsdottir , Valur Emilsson , Shyamali Ghosh , Adam Baker , Steinunn Snorradottir , Hjordis Bjarnason , Maggie C Y Ng , Torben Hansen , Yu Bagger , Robert L Wilensky , Muredach P Reilly , Adebowale Adeyemo , Yuanxiu Chen , Jie Zhou , Vilmundur Gudnason , Guanjie Chen , Hanxia Huang , Kerrie Lashley , Ayo Doumatey , Wing-Yee So , Ronald C Y Ma , Gitte Andersen , Knut Borch-Johnsen , Torben Jorgensen , Jana V van Vliet-Ostaptchouk , Marten H Hofker , Cisca Wijmenga , Claus Christiansen , Daniel J Rader , Charles Rotimi , Mark Gurney , Juliana C N Chan , Oluf Pedersen , Gunnar Sigurdsson , Jeffrey R Gulcher , Unnur Thorsteinsdottir , Augustine Kong & Kari Stefansson

We conducted a genome-wide association study for type 2 diabetes (T2D) in Icelandic cases and controls, and we found that a previously described variant in the transcription factor 7-like 2 gene (TCF7L2) gene conferred the most significant risk. In addition to confirming two recently identified risk variants, we identified a variant in the CDKAL1 gene that was associated with T2D in individuals of European ancestry (allele-specific odds ratio (OR) = 1.20 (95% confidence interval, 1.13–1.27), P = 7.7 |[times]| 10|[minus]|9) and individuals from Hong Kong of Han Chinese ancestry (OR = 1.25 (1.11–1.40), P = 0.00018).