On one hand, as an endothelial-related inflammatory mediator, increased YKL-40 may contribute to activation of endothelial cells to express vascular adhesion molecule-1 and intercellular adhesion molecule-1, further damaging vascular smooth muscle cells and endothelial cells, as well as accelerating the progression of atherosclerosis and plaque rupture [12]. This evidence concerns the gene CHI3L1 and atherosclerosis.