At a molecular level, FFAs activate nuclear factor-κB (NF-κB) via their ligation of Toll-like receptor 4 (TLR4), leading to release of pro-inflammatory cytokines, including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), and the formation of reactive oxygen species (ROS) (3), suggesting that the abnormal elevation of circulating FFAs may cause endothelial dysfunction by inducing inflammation and oxidative stress in vascular tissues. The gene discussed is TLR4; the disease is endothelial dysfunction.