CYP2E1-mediated ROS can also stimulate endotoxemia and elevate serum levels of LPS, which can travel to the liver, upregulating pro-inflammatory mediators, including tumor necrosis factor-alpha (TNF-α) [61] and hypoxia-inducible factor 1-alpha (HIF1-α) [49]. This evidence concerns the gene HIF1A and serum lipopolysaccharide activity.