It should be noted that all of the mice in this study received the HFD to induce obesity and its metabolic comorbidities, and although we did not measure fasting glucose or insulin concentrations prior to the change in diet, the fasting glucose and insulin concentrations of all mice post-HFD were elevated compared with chow-fed mice of a similar age, regardless of exposures. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.