Other researchers observed that SMAD knockout mice were protected from diet-induced obesity and DM, that elevated concentrations of TGFβ1 increases the risk of developing type-2 DM, that SMAD proteins are involved in obesity-induced glucose, and that lipid abnormalities support the role of TGFβ1 signaling in the pathogenesis of insulin resistance and DM [22,26,62,63,64]. The gene discussed is TGFB1; the disease is obesity due to melanocortin 4 receptor deficiency.