Overproduction of elastolytic enzymes and/or a decrease of some of their inhibitors are frequently associated with inflammatory conditions where the release of elastin fragments with chemotactic properties for monocyte contributes to structural deterioration (e.g., atherosclerosis), enlargement and eventual rupture of large vessels (e.g., aortic aneurysms) and promote osteogenic differentiation and subsequent calcification (1, 23, 164, 165). The gene discussed is ELN; the disease is atherosclerosis.