Recent large scale clinical trials have demonstrated that a substantial proportion of patients with psychotic disorders, such as schizophrenia and bipolar disorder, discontinue their antipsychotic medications due to either lack of efficacy or intolerable side effects, especially extrapyramidal symptoms (EPS). In clinical practice, it is essentially a trial and error process in deciding the best antipsychotic drug to start or switch to after a failed trial as there is little empirical data available to guide clinicians in drug selection. One promising tool, which can potentially provide valuable information to help guide medication management, is pharmacogenetic analysis of cytochrome P450 enzymes that metabolize most antipsychotics. CYP450 is a family of liver enzymes responsible for metabolizing many drugs and toxins. Genes coding for some of these enzymes have many polymorphisms, some of which produce essentially non-functional enzymes that result in poor metabolism of drugs. For example, CYP2D6 has more than 70 known mutations. Poor metabolizers may have a higher plasma concentration of a particular drug at usual dosages, which may lead to more severe side effects and potential drug discontinuation. On the other hand, rapid metabolizers tend to have a lower drug concentration in the body and may require a higher-than-usual dose to achieve clinical efficacy.