Attention deficit hyperactivity disorder (ADHD) is a common neuropsychiatric disorder of childhood, affecting 5% of school-aged children worldwide (Polanczyk et al., 2007), and persisting into adulthood in 30-50% of cases (Faraone and Biederman, 2005; Polanczyk et al., 2007). The disorder, characterised by high levels of inattention, uncontrollable hyperactivity, and impulsivity, is classified into three clinical subtypes: predominantly inattentive, predominantly hyperactive, and combined (American Psychiatric Association, 2013). ADHD is reported more often in males than females, with population and clinical studies showing male:female ratios of 4:1 and 9:1 respectively (Biederman et al., 2002; Cuffe et al., 2005). The disorder has been shown to have negative impacts on family relations and academic functioning (Mannuzza et al., 1993), and is associated with a greater likelihood of risk taking behaviours and drug use (Konstenius et al., 2015). The aetiology of ADHD remains poorly understood, although both environmental and genetic factors are known to contribute to the onset of the disorder. Environmental factors such as prenatal exposure to alcohol, cigarettes, and illicit drugs have all been associated with an increased risk of ADHD (Banerjee et al., 2007; Langley et al., 2005; Sagiv et al., 2013). Low birth weight and adverse life experiences have also demonstrated associations (Banerjee et al., 2007; Heinonen et al., 2010). Despite this, only a small portion of the aetiology of ADHD can be explained by environmental factors. Family and twin studies provide estimates of heritability at around 76% (Faraone et al., 2005). Furthermore, concordance rates in monozygotic (MZ) twins are consistently higher than those in dizygotic (DZ) twins (~80% and ~40%, respectively; Levy et al., 1997). There is, therefore, a significant genetic contribution to ADHD risk. Research into the genetic basis of ADHD initially focussed on candidate genes identified from animal models or knowledge of drug targets. In particular, genes involved in catecholamine (dopamine, noradrenaline) and serotonin transmission have been thought to be important to the aetiology of ADHD, and several of these have demonstrated replicable evidence of association (Faraone and Biederman, 2002; Gizer et al., 2009). More recently, hypothesis free genome wide association studies (GWAS) have been used to identify single nucleotide polymorphisms (SNPs), and copy number variations (CNVs) associated with the disorder. These approaches scan the genomes of cases and control individuals for thousands of SNPs to determine if any SNPs or CNVs (as identified by consecutive sets of SNPs) are associated with the disorder.