With the onset of adverse clinical vascular events, the activated cells within the plaque secreted matrix proteases that degraded extracellular matrix proteins and weakened the fibrous cap, resulting in rupture and thrombus formation.[23] In our previous pilot study on profiling gene expression in peripheral blood of AMI patients, we found that AMI patients had a lower expression of PIK3C2A than non-CHD patients. This evidence concerns the gene PIK3C2A and coronary artery disorder.