Conversely, a protective role for TIMP-3 on AAAs has been highlighted in both non-atherosclerotic and atherosclerotic mice Ang II-induced AAA mouse models, with both approaches demonstrating that Timp3-deficiency adversely affected vascular remodeling through increased inflammation and proteolytic activity, and consequently contributing to reduced collagen and elastin contents [47,48]. This evidence concerns the gene TIMP3 and achalasia-alacrima syndrome.