It has been suggested previously that mice treated with Ldlr-ASO could develop less atherosclerosis than Ldlr−/− mice because Ldlr-ASO, which strongly targets the liver, is unlikely to reduce Ldlr expression in other Ldlr-expressing cells such as macrophages (9), thereby impacting lesion development (23, 24). This evidence concerns the gene LDLR and atherosclerosis.