Apart from the effects on dampening proinflammatory response and inhibiting pyroptosis, many other mechanisms, such as supporting the energetic metabolism of mitochondrion coupled with activating the biogenesis of mitochondria, reducing the levels of cardiac contractile proteins, inhibiting the activation of NF-κB, downregulating the expression of the TLR4/myeloid differentiation factor-2 (MD2) complex on myeloid cells, suppressing the overactivation of platelets and enhancing autophagy, also contribute to the protective actions of CO in sepsis and endotoxemia [124,125,126,127,128,129]. This evidence concerns the gene TLR4 and Sepsis.