There was also an increased incidence of elastin degradation, greater fibrotic burden, phenotypic switching of VSMC (ie, α-SMA–expressing myofibroblasts), and greater severity of AAA with formation of a false lumen.27 This exacerbation of multiple hallmarks of aneurysmal disease confirms the capacity of CNP to dampen many pathways that promote AA pathogenesis. The gene discussed is ELN; the disease is triple-A syndrome.