Numerous epidemiological studies indicate that obesity and type 2 diabetes significantly increase breast cancer risk and mortality. The molecular mechanisms implicated in this association remain poorly understood. By employing a nonobese model of type 2 diabetes, Novosyadlyy and colleagues show that type 2 diabetes accelerates mammary gland development, formation of hyperplastic precancerous lesions, and malignant tumor growth independent of obesity. Furthermore, the authors demonstrate that hyperinsulinemia acting through the insulin and IGF-I receptors is a key pathophysiological mechanism promoting tumor development in the context of type 2 diabetes. Finally, the authors propose that interventions aimed at reducing insulin levels and signaling may delay the onset of cancer in patients with type 2 diabetes and will have an enormously positive public health impact. For details, see the article by Novosyadlyy and colleagues on page 741 of this issue.