Indeed, LXR activation both in vitro and in vivo has been shown to down-regulate the production of pro-inflammatory cytokines such as IL-1β, Il-6, and tumor necrosis factor alpha (TNFα) in macrophages under lipopolysaccharide (LPS) or bacterial stimulation and in models of contact dermatitis, atherosclerosis, lung inflammation, and neuroinflammation [11,12,14,15,40,41]. This evidence concerns the gene TNF and atherosclerosis.