Attention-deficit hyperactivity disorder (ADHD), a childhood-onset disorder, is characterised by severe and impairing inattention, motor hyperactivity, and impulsiveness.1,2 It affects around 2% of children and most of those affected continue to show impairment in adult life.1,2 Although ADHD is highly heritable, no specific susceptibility genes have been unequivocally identified.1,2 Despite high heritability, neurodevelopmental features, and associated learning difficulties, some persist in arguing that the disorder is mainly a social construct.3,4 There is now clear evidence that submicroscopic chromosomal structural abnormalities, often referred to as copy number variants (CNVs), are an important source of genetic variation,5 and that large, rare CNVs contribute to other neurodevelopmental disorders including intellectual disability, schizophrenia, and autism.6–11 Although some have postulated that rare CNVs might be involved in ADHD,12 no specific variant has yet been implicated in the disorder, and there are as yet no reports of an increased burden of CNVs in ADHD.
