However, some inflammatory stimuli, including TNF-α, interleukin-1βLPS, downregulate eNOS expression by decreasing mRNA stability, which is blocked by NF-κB inhibition,9 such that eNOS has been defined as an NF-κB-responsive negative gene.9 In this present study, we showed that CO prevents TNF-α-mediated decreases in eNOS expression, which precludes the inflammation-induced endothelial dysfunction associated with the pathogenesis of cardiovascular diseases. This evidence concerns the gene NFKB1 and cardiovascular disorder.