These agents included statins; niacin (20% reduction of Lp(a) at maximal dose but with an unknown effectiveness in reducing major atherosclerotic cardiovascular events-MACE) [221]; cholesteryl ester transfer protein (20–30% reduction of Lp(a) with no reduction in MACE) [222]; and apolipoprotein B100 antisense oligonucleotide mipomersen (20–40% reduction in Lp(a) levels but MACE reduction unknown in patients with elevated Lp(a) with significant concerns regarding potential hepatotoxicity which justifies limited approval for homozygous familiar hypercholesterolemia) [223]. The gene discussed is LPA; the disease is familial hypercholesterolemia.