Functionally, A1M enhances MQs migration as well as the proinflammatory response in cardiac fibroblasts and MQs in vitro, intramyocardial administration of recombinant murine A1M augment MQs infiltration, inflammation, and matrix metalloproteinase-9 (MMP-9) mRNA expression in the infarct and border zones, disturbs fibrotic repair, and drives cardiac rupture during the acute phase of MI in vivo [89]. The gene discussed is MMP9; the disease is myocardial infarction.