Polymorphisms, genetic variations with a frequency of greater than 1% of the population, or mutations, a change in genetic sequences in less than 1% of the population, can affect patient therapeutic response or metabolism of a given drug (Meyer, 2000). Genetic polymorphism may also refer to the occurrence in a population of more than one allele at the same locus with the least frequent allele occurring more frequently than can be accounted for by mutation alone. Less precisely, genetic polymorphism is described as differences in DNA sequence among individuals, groups, or populations that gives rise to different phenotypic forms such as the human blood groups or other body characteristics. Genetic polymorphism can occur with drug metabolism enzymes, drug transporters, and even drug receptors that govern therapeutic responses of drugs. Therefore, it is rational to individualize dose regimens based on pharmacokinetic data obtained from different polymorphic groups. Many alleles encoding different drug receptors are being discovered and studied with increasing frequency. Pharmacokinetic parameters influenced by genetic differences include drug bioavailability, distribution, metabolism, and tissue binding. Environmental factors (eg, smoking, drug–drug interactions, nutritional status) and pathophysiology of the patient (eg, cardiovascular disease, age, hepatic and renal disease) can also influence the pharmacokinetics of a drug. Our understanding of the impact of these genetic differences on clinical pharmacokinetics and pharmacodynamics is in its infancy.