A last aspect to be discussed relates to the genetic models currently used in ADHD research. Up to now, we work under the assumption that the ‘common disease, common variant’ model will hold for ADHD. This model suggests that ADHD is caused by multiple variants that are common in the population and each contribute a small amount of disease risk. However, experience from GWAS in other multifactorial disorders now challenges this view and postulates the existence of rare genetic variants contributing to disease, that are not captured by GWAS (see also McCarthy et al. 2008 for a more elaborate discussion of this subject). This case of the ‘missing heritability’ might imply that private or low-frequency variants of large effect size exist and actually explain most of the heritability of a multifactorial disorder in individual patients. Copy number variants (CNVs) might contribute a part of this puzzle. CNVs include insertions, deletions and duplications and encompass relatively large genomic segments of 1 kb to several Mb in size (Redon et al. 2006; Sebat et al. 2004). Although they are a frequent class
