This result suggests that riboflavin could reduce obesity-related hypoadiponectinemia and, at least in part, explain lower pro-inflammatory activation and reduced release of TNFα, IL-6 and HMGB1 as well as NFκB phosphorylation because of the improvement of the action of adiponectin, an important inflammation controller [23]. The gene discussed is HMGB1; the disease is adiponectin deficiency.