A recent study found that soda intake increased inflammatory mediators such as C-reactive protein, IL-6, and tumor necrosis factor receptor 2 concentrations.[39] In addition, soda intake induces obesity and elevates inflammatory biomarkers for high glycemic load by rapidly increasing blood glucose.[40] These results provide a possible explanation for the potential pathogenesis of OA due to soft drinks. Here, TNFRSF1B is linked to obesity due to melanocortin 4 receptor deficiency.