In addition to the bacterial immune response mediated by TLR4, viral infections also activate pattern recognition receptors (PRRs) and trigger a specific cellular signaling pathway that terminates with the activation of c-Jun N-terminal kinase (JNK), inhibitor of nuclear factor-κB kinase subunit β (IKKβ), NF-κB, and transcription of proinflammatory cytokines, which are mediators of insulin resistance. This evidence concerns the gene TLR4 and Insulin resistance.