Patients with familial hypercholesterolemia, who have a severely increased low-density lipoprotein (LDL) cholesterol level from birth and are at high risk for premature cardiovascular disease, have inspired and contributed to major advances in lipid therapeutics. A notable example is the drug class targeting proprotein convertase subtilisin–kexin type 9 (PCSK9). Overactivity of PCSK9, which promotes LDL receptor degradation, was discovered to be a cause of familial hypercholesterolemia. 1 The addition of a PCSK9 inhibitor to statin therapy can lower the LDL cholesterol level by 60% and reduce cardiovascular risk. 2 Reduction of cardiovascular risk with PCSK9 inhibitors is correlated with absolute lowering of . . .