The role of TIMP-3 in the formation of AAA has been explored in the non-atherosclerotic and atherosclerotic Ang II-induced AAA mouse model, with both approaches demonstrating Timp3-deficiency adversely affected vascular remodelling through increased inflammation and proteolytic activity, consequently contributing to reduced collagen and elastin content (32, 134), highlighting the protective role of TIMP-3 on AAAs. The gene discussed is AGT; the disease is achalasia-alacrima syndrome.