Clopidogrel is key to antiplatelet therapy, but it must be converted to an active metabolite by CYP2C19 and other enzymes to exert its drug action. In clinical settings, the factors that may influence the therapeutic efficacy of clopidogrel include high basal platelet activity, drug-drug interactions, poor medication compliance, and genetic variation. Genetic variation impacts the metabolism of clopidogrel. If defective alleles of CYP2C19 (e.g., CYP2C19*2) are present, poor metabolism of clopidogrel will result and affect its clinical efficacy. In such cases, the recommended alternative is switching to other antiplatelet agents such as prasugrel.