NFKB1 and atherosclerosis: TNF-α, adhesion molecules VCAM-1 and ICAM-1, ROS generated from NADPH oxidase, and other proinflammatory molecules increase the production and expression of LOX-1; on the contrary, the suppression of the inflammatory NF-kB pathway downregulates its expression, thus limiting the formation of foam cells and preventing atherosclerosis [21].