Classical and Mendelian epidemiological studies demonstrate that elevated plasma concentrations of lipoprotein(a) (Lp(a)) may be related to the development of atherosclerotic cardiovascular disease (ASCVD).1, 2, 3, 4, 5 The pathobiology appears to entail the infiltration of Lp(a) into the subendothelial space, where it may promote foam cell formation, oxidative stress, inflammation, and thrombosis.2 However, the metabolism of Lp(a) in humans remains enigmatic and requires clarification to enhance the clinical understanding of this major heritable risk factor. This evidence concerns the gene LPA and atherosclerosis.