Highlights of the first section include the initial chapter describing behavioral phenotypes, with a detailed historical perspective that only James Harris can do, in his erudite and informative style. Each chapter covers a neurodevelopmental disorder and includes the latest data on genetic information and genotype-phenotype correlations. In the chapter on Smith-Magenis syndrome, Andrea Gropman and Ann Smith not only cover flanking genes well, and these genes' additive features to the phenotype, but they also discuss general mechanisms of deletion that occur across disorders. Walter Kaufmann does an outstanding job in covering the expanded phenotypes of not only fragile X syndrome caused by the full mutation at FMR1 but also by premutation disorders, which includes their association with autism spectrum disorder, attention deficit hyperactivity disorder (ADHD), and adult neurodegeneration leading to the fragile X-associated tremor ataxia syndrome. Kaufmann's discussion of the association of fragile X syndrome and autism is thorough and reflects his excellent research covering the relationship of social anxiety, social withdrawal, and autism spectrum disorder. George Capone excels in his discussion of frontal-caudate/putamen-thalamic circuits and their relationship to stereotypic behavior in Down syndrome. His discussion is pertinent to many other neurodevelopmental disorders that involve executive function deficits and ADHD. His description of neurobiological events "that are played out in utero and continue to reverberate with lifelong repercussions for cognitive, behavioral and emotional function" is true for most of the neurogenetic disorders. Travis Thompson reviews endophenotype similarities between Prader-Willi syndrome and autism and helps us understand the commonalities across disorders as they relate to autistic features of stereotypes, social avoidance, and social deficits. Carolyn Mervis and Angela John cover Williams syndrome, and their historical perspective of the controversy regarding the modularity of language as differentiated from intellectual abilities is exceptional. They relate detailed neuropsychological studies to new magnetic resonance imaging studies. These studies have found that the reduced sulcal depth of gray matter in the extraparietal sulcus serves as a roadblock to dorsal stream processing in this syndrome. This may explain the visual spatial constructional deficits and perhaps the relational language deficits seen in Williams syndrome. There may be a central processing center for spatial, temporal, and quantitative processing that is affected not only in Williams syndrome but also in other neurodevelopmental disorders.