Effective platelet inhibition has become a cornerstone in the management of patients with acute coronary syndrome (ACS). The addition of clopidogrel to aspirin has provided significant reductions in major cardiovascular events in patients with ACS in general, and particularly among those treated invasively by percutaneous coronary intervention (PCI).1 Yet studies have demonstrated that the therapeutic response of clopidogrel is variable among patients,2 and low or incomplete platelet inhibition has been associated with increased risk for major adverse cardiovascular events.3