Attention-deficit hyperactivity disorder (ADHD) and related symptom dimensions of inattention and hyperactivity have been shown to be more prevalent in the relatives of probands with ADHD than in relatives of controls. This familiality has been shown to be heritable in both twin studies and segregation analyses with models ranging from a major autosomal dominant gene with reduced penetrance to additive genetic factors. All models have included substantial environmental and genetic components. Like other relatively common diseases, ADHD is likely to be heterogeneous in terms of degree of genetic risk from family to family and the genes contributing to susceptibility. Several genes are likely to contribute to both susceptibility and protection. For example, genetic variation (as well as environmental variation) may contribute to the excellent outcome of a substantial proportion of children with ADHD. Until recently, it has been difficult to move from estimates of genetic influence to determining which specific genes contribute to complex genetic disorders like ADHD. However, recent advances in both molecular genetics and statistical analysis allow testing of both candidate genes and screening for genes throughout the genome for which no previous reason is present to test them specifically. Although relatively few studies have been conducted relative to other complex genetic disorders, there are replicated linkage disequilibrium and linkage findings in ADHD for the dopamine transporter (DAT) and dopamine D 4 receptor (DRD4) genes. It is now possible to begin to understand how these findings correlate with the heterogeneity within the syndrome of ADHD and how they relate to other neurobiological studies of ADHD. Using information from current molecular genetic findings and those expected from genome-wide linkage studies, it may become feasible to develop new medication treatments and to develop animal models for the purpose of understanding more about the developmental neurobiological mechanisms leading to ADHD and related disorders. Furthermore, it may become possible to target children at relatively higher genetic risk of ADHD for prevention/early intervention, such as provision of intensive parent training for infants or toddlers at high risk of ADHD and related disorders.