, Volume 50, Issue 1, pp 1-4,
Open Access This content is freely available online to anyone, anywhere at any time.
Date: 10 Nov 2006

TCF7L2: the biggest story in diabetes genetics since HLA?

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Much has been made over the past decade of the potential for genetics to advance our understanding of the pathogenesis of type 2 diabetes and to ‘revolutionise’ management of this condition [1]. Others have argued that these claims are premature [2]; indeed, some have questioned the contribution of genetic predisposition to the pathogenesis of common forms of type 2 diabetes [3].

In the case of relatively uncommon monogenic and syndromic forms of diabetes, such as maturity onset diabetes of the young (MODY) and neonatal diabetes, identification of rare causal mutations has delivered both knowledge and clinical translation [4, 5]. In contrast, progress in unravelling the genetic architecture of more typical, common, multifactorial type 2 diabetes has been painfully slow [6]. The reasons have been well-rehearsed [7]. The complex web of susceptibility factors—genetic, environmental, social—that contributes to individual risk of developing type 2 diabetes means that most predisposing geneti