Further, antisense oligonucleotides (ASOs)-induced loss of FADS1 activity in low-density lipoprotein receptor (LDLR) null mice promotes hepatic inflammation, hypercholesterolemia, and atherosclerosis, and increases hepatic free cholesterol and cholesterol ester levels, but reduces hepatic triglyceride in an n3 substrate fatty acid-enriched diet [18]. This evidence concerns the gene LDLR and familial hypercholesterolemia.