Dasu et al. previously described that TLR2 and TLR4 were increased in monocytes from type 2 diabetic patients and importantly, that HA molecules as well as some of other tissue-damaged associated molecules (HMGB1 and HSP61), co-immunoprecipitated with these receptors and might be linked to their activation through the TLR/NF-κB-dependent pathway [19]. The gene discussed is TLR4; the disease is type 2 diabetes mellitus.