In addition to being some of the first to report on the molecular mechanisms through which Lp(a) causes aortic valve calcification or CAVS, these studies suggest that in addition to promoting CAVS and inflammation through its oxidized phospholipids (OxPL) content, the proatherogenic properties of Lp(a) could be mediated by proteins and enzymes carried by this unique lipoprotein. This evidence concerns the gene LPA and aortic valve calcification.