Whether a plaque develops into a vulnerable one, with increased risk of atherothrombotic complications, largely depends on its phenotype.2 The ECM remodelling process in the arterial wall involves the synthesis and breakdown of ECM proteins such as collagens, proteoglycans and elastin.3 Excessive or uncontrolled ECM remodelling in CAD has been proposed by previous studies showing that ECM-degrading enzymes, such as matrix metalloproteinases (MMPs), are upregulated in rupture-prone plaques.4–6 Also, circulating levels of MMPs, particularly MMP-9, have been shown to predict the risk of CAD.7 8. Here, MMP9 is linked to coronary artery disorder.