JUN and achalasia-alacrima syndrome: 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.