ELN and Marfan syndrome: Studies have shown that disordered elastogenesis is active in matrix remodelling in AAA15 and Marfan’s syndrome.16,17 However, newly synthesized tropoelastin monomers secreted from vascular smooth muscle cells 18–20 and macrophages21 frequently fail to cross-link into polymeric elastin fibres12,21–23 as a result of the reduced expression, absence or inactivation of LOX24–29 or any of the components of the microfibrillar scaffold required for fibre assembly.30–32