Recent studies have suggested that adipokines such as leptin, adiponectin and resistin, produced by adipocytes and dysregulated in obesity and metabolic syndrome, as well as tumour necrosis factor alpha (TNF-α), a multifunctional cytokine and adipokine, are key mediators that link obesity and its associated chronic inflammatory milieu with the pathogenesis of PsD. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.