Looking at the processes potentially involved in the etiology of ADHD, little evidence (as yet) points to a direct involvement of neurotransmitters (at least the classic dopaminergic, noradrenergic and serotonergic pathways) or regulators of neurotransmission (except for DNM1). Some suggestions are found for involvement of ‘new’ neurotransmission and cell–cell communication systems, though, like glutamate, vasopressin, and TAFA proteins. Also, the potential involvement of potassium channel subunits and regulators definitely warrants further investigation. However, more basic processes also seem involved, like cell division, adhesion (especially via cadherin and integrin systems), neuronal migration, and neuronal plasticity, as well as related transcription, cell polarity and extracellular matrix regulation, and cytoskeletal remodeling processes. Our conclusion is consistent with and extends the conclusion drawn by Lesch and coworkers based on the findings from their GWAS, in which they suggest that neuronal spine formation and plasticity may underlie the pathophysiology of ADHD. Finding inflammatory genes (IL16 and ADAMTS2) is somewhat surprising, although inflammation is already known to be involved in different psychiatric disorders, like major depression and Alzheimer’s disease (Anisman 2009; Bazar et al. 2006; Garcia-Bueno
