Therefore, the upregulation of melatonin observed in the placebo might be due to the endogenous melatonin synthesis to counteract obesity-associated inflammation as evidenced by the strong correlation between Δ melatonin and Δ IFNγ found only in the placebo group (r = 0.54, p = 0.02). The gene discussed is IFNG; the disease is obesity due to melanocortin 4 receptor deficiency.