Many reasons can explain nonresponsiveness to antiplatelet medications, such as interindividual variability in the metabolism of clopidogrel (which is a prodrug activated by CYP-3A4, CYP-2C19, and CYP1A2), drug-drug interactions (i.e., interaction on the same metabolic pathway for clopidogrel, but also competition for binding sites on COX-1 by nonsteroidal anti-inflammatory medications and aspirin), P2Y12 receptor polymorphisms and increased platelet turnover during inflammation, acute coronary events, and diabetes mellitus. The gene discussed is CYP2C19; the disease is diabetes mellitus.