Moreover, in a case-control animal study of LPS-induced sepsis, Li et al. demonstrated that LPS promoted cardiomyocyte death (apoptosis and pyroptosis) and enhanced the expression of pro-inflammatory mediators through the Toll-like receptor 4 (TLR4) and the NF-kB signaling pathway and the formation of the inflammasome NOD-like receptor protein 3 (NLRP3). This evidence concerns the gene NFKB1 and Sepsis.