The effects of antileukemic drugs are determined by the interplay of numerous gene products that influence each medication’s pharmacokinetics (drug metabolism or disposition) and pharmacodynamics (drug efficacy or toxicity). Specifically, pharmacogenetics focuses on genetic variation of drug metabolizing enzymes, targets and transporters and how these genetic variations interact to produce specific drug related phenotypes. Furthermore, potential genetic markers may serve to functionally sub-classify patients for their disease and therefore influence the nature and intensity treatment. These genetic markers may indicate novel drug targets or modifiers that may positively influence drug effects and toxicity, (such as reverse drug resistance and increased cellular uptake)1. Ultimately, the intent of pharmacogenetics is to develop polygenic models that accurately predict drug response and toxicity for individual patients, and to use these models to prospectively personalize treatment regimens with the goal of enhancing efficacy and safety through better understanding of the patient’s pharmacogenetic characteristics (Figure 1). Of note, pharmacogenomics is often considered synonymous with pharmacogenetics, but this latter term is increasingly used in the context of polygenic models that describe specific drug response phenotypes.