Genetic studies in mice have shown that interruption of NF-κB activity in hepatocytes and macrophages attenuates the development of insulin resistance in the setting of obesity.9 Thus, the development and progression of diabetes in obese individuals stems, in part, from these proinflammatory alterations that limit the response to insulin. This evidence concerns the gene NFKB1 and obesity due to melanocortin 4 receptor deficiency.