Since n-3 LC-PUFA upregulate PPARα, hepatic fatty acid oxidation has the potential to occur within the liver, and, since more apo B-100 is secreted out of the liver, less VLDL is synthesized, with the result of less of this harmful cholesterol entering the bloodstream, where the downstream further effects on the development of atherosclerosis are attenuated [94]. The gene discussed is PPARA; the disease is atherosclerosis.