Asthma is a common respiratory syndrome characterized by partially reversible airflow obstruction, airway hyperresponsiveness, and airway inflammation. The syndrome is caused by a complex interaction between genetic and environmental factors that results in a spectrum of biologic and clinical features. Among the spectrum of features is a highly variable response to asthma therapeutics. There are currently three major classes of asthma therapeutics available:(1) beta2-agonists (-agonist);(2) glucocorticoids (GC); and (3) inhibitors of the cysteinyl-leukotriene pathway (cLI). Asthmatic patients vary greatly in their response to all three classes of drugs and it is estimated that up to 60–80% of this variability may have a pharmacogenetic basis. Over the past 10 years, several polymorphic loci have been discovered in genes that play a role in the action of these drugs. Data suggest that these polymorphisms directly or indirectly alter an asthmatic’s response to therapy and can be used to predict the response to certain asthma drugs, thereby maximizing efficacy and avoiding adverse effects. It is likely that many, as yet undiscovered, polymorphisms exist given the large number of gene products involved in the pharmacodynamic and pharmacokinetic pathways of all three classes of asthma drugs. In this review we discuss the established asthma pharmacogenetic loci and describe a candidate gene approach that is being used to uncover additional polymorphisms with pharmacogenetic potential.