Since it has been suggested that the novel GLP-1/FGF21 axis plays a critical role in mediating the beneficial effects of GLP-1-based pharmacotherapy in people with obesity [150], these overall findings allow the hypothesis that FGF21 likely suppresses fetuin-A levels directly by acting on adipocytes through the upregulation of adiponectin levels mediated by PPARy activation. The gene discussed is AHSG; the disease is obesity due to melanocortin 4 receptor deficiency.