In a rat sepsis model generated via cecal ligation and puncture (CLP), SO2 supplementation significantly inhibited the CLP-induced expression of Toll-like receptors-4 and pyrin domain-containing protein 3 (NLRP3) in rat myocardial tissues, and SO2 exerted anti-inflammatory effects through the NLRP3 inflammasome signaling pathway, thereby attenuating sepsis-induced cardiac dysfunction (25). The gene discussed is TLR4; the disease is Sepsis.