Although these studies did not find that increased Lp(a) levels directly cause endothelial dysfunction or atherosclerosis progression, they enriched the understanding of how Lp(a) contributes to cardiovascular disease development [6,7]. However, recent research has shown the opposite, indicating that elevated Lp(a) levels can negatively impact endothelial function by interfering with lipoprotein transport, increasing adhesion reactions, and reducing vasodilator function [6]. This evidence concerns the gene LPA and atherosclerosis.