Activated monocytes release proteolytic enzymes, such as matrix metalloproteases that promote extracellular matrix degradation and make the plaque vulnerable.[29] In vivo, angiopoietin-2 blocking antibodies can reduce early atherosclerotic plaque development in mice.[16] Additionally, Ang-2 may enhance the formation of new vessels within the plaque and accelerate its progress.[15] Ang-2 counteracts the anti-inflammatory and anti-arteriosclerosis effect of Ang-1,[30,31] which may severely impede the endothelial healing process. This evidence concerns the gene ANGPT1 and arteriosclerosis disorder.