ASD is considered by many to be a genetically determined disorder; three well-known twin studies [6-8] estimate heritability at about 90% [9]. Sibling concordance varies from about 3 to 14%; linkage studies are consistent with a polygenic mode of transmission [10]. The 2008 finding by the Autism Consortium of a microduplication at 16p11.2 (1% of studied cases) raised hopes that a full ASD genomic pattern might soon be elucidated. However, more recent data suggest the heterogeneity and complexity of genetic abnormalities identified in children with ASD. Sakai et al. [11] set out with 26 ASD associated genes and then described an "interactome" of autism-associated proteins that may be necessary to describe common mechanisms underlying ASD. Voineagu et al. [12] provided strong evidence to suggest widespread transcriptional and splicing dysregulation as the key mechanism underlying brain dysfunction in ASD. On the basis of a detailed study of twins with autism, Hallmayer et al. [9] recently reported, as expected, high twin concordance yet also concluded that ASD has, in addition to moderate heritability, a substantial environmental component. Thus, studies to date suggest
