Wong et al. in an extensive review on the argument, underlined how metabolic syndrome, TLR expression and inflammation are linked in a way that MetS triggers TLR activation via several mechanisms including AGEs, FFAs, HMGB1, HSPs, and endotoxins, and TLR activation in turn leads to inflammation via MyD88 and TRIF dependent pathways.9 Here, HMGB1 is linked to metabolic syndrome.