Walking a fine line between β-cell secretion and proliferation.

Of the many common genetic variants associated with type 2 diabetes, that in TCF7L2 remains the most studied because it has the greatest effect size. However, the mechanism by which this variant alters diabetes risk remains elusive. A new study adds another layer of complexity, suggesting that the effects of TCF7L2 are context-dependent, and highlights a novel interaction that might bias a β-cell to a secretory or proliferative phenotype. This in turn might open up new avenues to the restoration of insulin secretion in people with type 2 diabetes.