Furthermore, there is evidence that large amounts of CoA can be released into the extracellular space after injury to the cell membrane or cell death in certain conditions such as heart attack, hypertension, and AS, modulating the function of cell surface receptors and acting as a competitive inhibitor of platelet aggregation, possibly preventing excessive thrombosis (Davaapil et al., 2014). This evidence concerns the gene CD177 and hypertensive disorder.