Current pharmacogenetic focus on genotype A number of clinically relevant drug metabo­ lizing enzymes (DMEs) are expressed poly­ morphically in the population, giving rise to at least three distinct genotypes; extensive metabolizers (EMs), poor metabolizers (PMs) and intermediate metabolizers. Depending on the number of copies of the functional wild­type allele inherited, there is an additional ultrar­ apid metabolizer (UM) genotype [1]. Clinically, the most relevant DMEs for pharmacogenetic studies are CYP2D6, CYP2C9, CYP2C19, UGT1A1 and TPMT. Pharmacokinetic studies show marked intergenotype variability in expo­ sure to certain drugs and their metabolites [2]. This variability may account for variability in drug response (efficacy and/or safety), depend­ ing on the pharmacological activities and the therapeutic indices of the parent compound and its metabolites. With the discovery of an ever increasing num­ ber of genetically determined variants of these DMEs, pharmacogenetic studies have focused on establishing associations between commonly prevalent DME genotypes and clinical outcomes (drug response or clinical phenotype) with the laudable aim of developing a dosing regimen appropriate to each genotype [3] – so­called per­ sonalized medicine. This individualization of drug therapy, displacing the traditional ‘one­size­ fits­all’ approach, is expected to make therapy not only more effective but also much safer. Currently, there is much interest in establish­ ing genotype–clinical outcome associations for high­profile drugs such as warfarin (metabolized by CYP2C9), tamoxifen (CYP2D6), clopido­ grel (CYP2C19), irinotecan (UGT1A1) and