Moreover, in myocardial extracts from humans and dogs, 90% of Ang-II-forming activity is accounted for by chymase (a serine endopeptidase) and not by ACE (a peptidyl-dipeptidase) [15], and chronic chymase inhibition attenuates the development of cardiac fibrosis and ventricular remodeling after experimental myocardial infarction [16]. Here, CMA1 is linked to myocardial infarction.