TLRs can induce the expression of proinflammatory cytokines through interactions with conserved pathogen-associated molecular patterns and subsequently activate nuclear factor-κB (NF-κB) signaling pathway, and produce proinflammatory cytokines in mammals, including humans.(13) Among the TLRs, TLR4 is strongly associated with T2DM, and plays a critical role in the pathogenesis of insulin resistance and T2DM.(14–16). This evidence concerns the gene TLR4 and Insulin resistance.