Asthma is a complex clinical syndrome with multiple genetic and environmental factors contributing to its phenotypic expression [1]. Multiple epidemiologic and experimental studies indicate that asthma risk may be modified by epigenetic changes, such as DNA methyl ation, covalent histone modifications, microRNA changes and chromatin alterations, after early or later environmental exposures [2]. This etiological heterogeneity adds to the complexity when addressing variation in the response to anti-asthma treatment. The relevant clinical variability in response to asthma medications may be due to genetic determinants and refers to the polymorphisms in the genes associated with asthma susceptibility, genes encoding either the drug targets or molecular components of the downstream signal transduction pathways responsible for drug action [3]. Clinically the spectrum of asthma severity has three distinct levels: mild, moderate and severe. At each level, the clinical characteristics and the mode of treatment of an individual differs (Figure 1). It is critical to determine the level of severity to better understand how to treat and control the asthma. Therapies typically used for the treatment of asthma include: β 2 -adrenergic agonists, for bronchodilation; glucortico steroids, for their potent anti-inflammatory action; theophylline and its derivatives, for bronchospasm and inflammation; and leukotriene inhibitors and antagonists as bronchodilators and antiinf lammatory drugs. Anticholinergics may also be used as bronchodilators, although they are less potent than β 2 -agonists. Short-acting β 2 -agonists (e.g., salbutamol, terbutaline, isoprenaline, fenoterol and so on) are the most effective medications used for the treatment of mild asthma, whereas long-acting β 2 -agonists (e.g., salmeterol, formoterol and so on), inhaled corticosteroids (ICs) and leukotriene inhibitors may be used independently or in combination for the treatment of mild-to-moderate asthma. Severe or ‘refractory’ asthma can be treated either by oral corticosteroids, by very high dose of inhaled corticosteroids or in combination with theophylline. The degree of responsiveness to these medications varies from person to person. Variability in an individual’s response to the prescribed asthma treatment may be due to several other factors, including treatment compliance, severity, intercurrent illness, environmental exposure, age and drug interactions with other medication being taken at the same time [4]. Although heterogeneity in treatment responses are likely to arise in part by environmental factors, it is thought that up to 60–80% of this variability may be due to genetic factors [5]. This indicates the need for finding genes responsible for clinically relevant variability in response to the main classes of asthma drugs. Many genetic variants often consist of just a single base pair substitution resulting in alterations of protein function or expression [6]. These SNPs, as well as their variable linear combinations (haplotypes), may be major determinants of the variability in therapeutic response.