Moreover, as shown by Luo et al., once the activity of the toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway was inhibited, iNOS became inactive, leading to an enhancement of vascular responsiveness and an increase in the survival of mice with CLP-induced sepsis (mean survival time increased from 1.7 days to 4.5 days) [109]. The gene discussed is NFKB1; the disease is Sepsis.