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Human genetics is revealing ever more variants that influence propensity to common diseases, but progress in translating these discoveries into the biological mechanisms responsible for predisposition continues to lag behind. A recent paper in Cell (Boj et al., 2012) using rodent models to examine how diabetes-associated variants near TCF7L2 perturb metabolic regulation provides surprising results.

Original publication

DOI

10.1016/j.cmet.2013.01.011

Type

Journal article

Journal

Cell Metab

Publication Date

05/02/2013

Volume

17

Pages

157 - 159