High Lp(a) plasma concentrations are associated with coronary heart disease, myocardial infarction, aortic valve calcification and stenosis, carotid atherosclerosis, stroke, and venous thromboembolism.1,2 Lp(a) concentrations are controlled mostly genetically by the LPA locus, which encodes apo(a) (apolipoprotein(a)) as the primary structural protein of Lp(a) and explains 70% to 90% of the Lp(a) concentrations.1 This evidence concerns the gene LPA and venous thromboembolism.