Furthermore, BAF60a, a component of the SWI/SNF complex, was upregulated in human and experimental mouse abdominal aortic aneurysm lesions, and genetic ablation of BAF60a in VSMCs was shown to attenuate AAA formation by inhibiting inflammation and extracellular matrix degradation in AAA mouse models induced by both Ang II infusion and elastase perfusion [197]. The gene discussed is SMARCD1; the disease is triple-A syndrome.