There have been more sequence changes [5] and potentially more selective events [53 and 54] in the chimp lineage than in ours. In fact, the statistical techniques for identifying accelerated regions have already been applied to other lineages [4• and 10]. The data and methods are already available to explore patterns of accelerated region evolution across the mammalian phylogeny. These studies will shed light on what, if anything, is uniquely human about the genes and pathways targeted by accelerated evolution in our species. Papers of particular interest, published within the period of review, have been highlighted as: • LDK378 of special interest This work was supported by the San Simeon Fund and institutional

funds from the Gladstone Institutes. “
“The publisher regrets that several errors appeared in the original paper. The correct text is below. In the abstract section, the fourth sentence should read as follows: As a result, we found that patients with ADHD PCI-32765 purchase had decreased ALFF in the right inferior frontal cortex and bilateral cerebellum and the vermis as well as increased ALFF in the right

anterior cingulated cortex, left sensorimotor cortex, and bilateral brainstem. In Fig. 3, the numbers beside the blue bar (upper) should be −3.828 and −2.796, respectively. And the numbers besides the red and yellow bar (lower) should be +2.796 and +4.604, respectively. “
“Current Opinion in Genetics & Development 2012, 22:229–237 This review comes from a themed issue on Molecular and genetic bases of disease Edited by Beverly Emanuel and Steve Warren For a complete overview see the Issue and the Editorial 0959-437X/$ – see front

matter, © 2012 Elsevier Ltd. All rights reserved. DOI 10.1016/j.gde.2012.03.002 else Autism spectrum disorder (Figure 1) is a lifelong developmental condition that affects about 1 in 110 individuals [1], with onset before the age of three years. It is characterized by abnormalities in communication, impaired social function, repetitive behaviors and restricted interests [2]. The presentation of autistic features is variable, with symptoms ranging from mild to severe, sometimes with poor clinical outcomes. These individuals vary greatly in cognitive development, with some who function well above average and others showing profound intellectual disability. In a clinical genetics setting, individuals with ASD or who exhibit autistic-like behaviors have become increasingly apparent [3]. One of the hallmarks of ASD is a 4:1 male to female gender bias, which may rise to 11:1 when considering Asperger disorder [4]. There is strong evidence for the importance of complex genetic factors comprised of different forms of genetic variation (or architecture) in the etiology of ASD (Figure 2). Earlier family studies [5, 6, 7 and 8] found 8–19% recurrence of ASD among sibs of affected probands.