As CAD severity has also been inversely associated with circulating HSP levels (44), the absence of CLEC3B and HSP90AA1 from the PR of STEMI patients may reflect circulating activated platelets and increased plaque uptake; however, the pathophysiological significance of these particular PR proteins in the peripheral circulation of CAD patients remains to be explored. The gene discussed is HSP90AA1; the disease is coronary artery disorder.