TNF-α, which is a risk factor for various inflammatory cardiovascular diseases, such as atherosclerosis, diabetic vascular complication and preeclampsia, causes endothelial dysfunction by suppressing eNOS expression.19, 20 By contrast, CO inhibits TNF-α-mediated inflammation and vascular dysfunction.21, 22 We examined whether CO regulates the eNOS/NO pathway in TNF-α-treated HUVECs. The gene discussed is NOS3; the disease is atherosclerosis.