This article reviews family, twin, and adoption studies, along with segregation analyses and molecular genetic studies, suggesting that both genetic and environmental factors contribute to the etiology of ADHD. Findings also indicate that the genetic mechanisms that predispose individuals to ADHD are likely to be complex, and the literature on ADHD raises many questions regarding clinical and pathophysiologic heterogeneity of the disorder. Although there is no single pathophysiologic profile of ADHD, data do implicate dysfunction in the frontosubcortical pathways that control attention and motor behavior. Moreover, the effectiveness of stimulants, along with animal models of hyperactivity, point to catecholamine dysregulation as at least one source of ADHD brain dysfunction.