NFKB1 and endothelial dysfunction: 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.