Pro-inflammatory factors like tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) are precipitating factors for the development of endothelial dysfunction in addition to ROS which restrain the bioactivity of nitric oxide and nitric oxide synthase by upregulating various atherosclerotic factors expression through the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. This evidence concerns the gene NFKB1 and endothelial dysfunction.