Moreover, SO2 decreased the level of inflammatory cytokines, inhibited TLR4 and NLRP3 expression, and reduced the inflammatory caspase-1 expression in the myocardial tissue of CLP rats and the LPS-treated primary neonatal rat cardiac ventricular myocytes (Yang et al., 2018), suggesting that NLRP3/caspase-1-mediated cell pyroptosis might also participate in the protective role of SO2 on the sepsis-induced cardiac dysfunction. The gene discussed is CASP1; the disease is Sepsis.