Circulating TGF-β1 levels have been shown to exhibit dependency on both intermittent hypoxia and obesity (mediated through serum leptin levels)19,21–23, and such observations lead to the question whether OSA may have any effect on the activation of the TGF-β1/SMAD pathway in patients with melanoma, and if so, whether there is any synergistic effect with obesity. The gene discussed is TGFB1; the disease is obesity due to melanocortin 4 receptor deficiency.