In the last 2 years, much progress has been made in identifying genes for psychiatric disorders through GWAS. From the studies so far it has become apparent that early power estimates have been far too optimistic and at least several thousands of samples will be needed for the design of an optimal study (Burton et al. 2008). Genetic heterogeneity appears even more extensive than previously expected, with relative risks due to single genetic variants in the range of 1.05–1.1 or even smaller (Ferreira et al. 2008; Neale et al. 2008a; O’Donovan et al. 2008; Sklar et al. 2008). ADHD is no exception to this, and so all of the ADHD GWAS performed to date are highly underpowered. In addition, Lesch and colleagues used a pooling design, which reduces power by about 70% and puts limitations to the genetic models that can be investigated (Lesch et al., 2008). Furthermore, using controls unscreened for the presence of psychiatric disorders can be expected to reduce power, though the effect of this is modest, given that the prevalence is at most 5% (McCarthy et