Interpatient variability among medication doses has been a long-standing obstacle for many prescribers. Some medications result in increased morbidity and mortality in a small percentage of the population. For many years, the cause of such toxicities was unknown. This mystery has been resolved by the discovery that the abscence or abnormality of specific genes that code for receptros, drug-treated proteins, drug transport mechanisms, and drug metabolizing enzymes could alter how an affected individual will respond to a given drug. One such incidence is the genetic polymorphism in thiopurine s-methytransferase (TPMT). In comprehending the mechanism of this polymorphism, it is important to understand the matabolic pathway of thiopurine drugs. Through study of this pathway, researchers began to look into whether other polymorphisms aside from TPMT could be a source of the dose-related toxicity with the thiopurines. The prospect that this polymorphism may contribute to an increase in number or exacerbation of side effects beyond the commonly presented bone marrow toxicity also has been visited. Becoming more aware of this genetic issue has presented the need to evaluate the cost effectiveness of genetic testing to counteract the expected cost of treating extreme myelosuppression. Having knowledge of new pharmacogenomic technology and the tests available can benefit pharmacists in any setting. Pharmacists will be more prepared to address patient concerns such as necessity and cost effectiveness.