In animal models of fatal endotoxemia or severe sepsis, heparin inhibited the LPS cytoplasmic transmission by blocking the hMGB1-LPS interactions and decreasing the heparinase-induced glycocalygeal degradation in macrophages, thereby attenuating the overactivation of this harmful cascade (Tang et al., 2021). This evidence concerns the gene HMGB1 and serum lipopolysaccharide activity.