In addition to arterial dilatation, AAAs are characterized by decreased medial elastin content and disruption or fragmentation of elastic lamellae,4 and MMPs, especially MMP-12, clearly play an important role in this context.37–40 Indeed, elastin preservation in the CaCl2 experimental model was observed in aortas of select Mmp-knockout mice38,41 and in mice treated systemically with a c-Jun N-terminal kinase inhibitor to hinder MMP production.42 Moreover, numerous studies have evaluated the effects of nonspecific MMP inhibitors in organ culture experiments or animal models of AAAs. Here, MMP12 is linked to achalasia-alacrima syndrome.