While defective LOX levels have been related to nonsyndromic aneurysms of ascending aorta, enhanced LOX and LOXL1 expression and higher LOX activity have been reported in the aorta from animal models and patients with Marfan syndrome, a systemic connective tissue disorder characterized by severe cardiovascular manifestations, including TAA, acute aortic dissections, and aortic ruptures [25]. This evidence concerns the gene LOX and connective tissue disorder.