GABA interneurons surround each minicolumn, and some genetic evidence and post mortem data suggest a GABAergic abnormality in ASD (Fatemi et al., 2002). Multiple genes involved in the development and function of the GABAergic system, including dlx5, have been involved in Rett syndrome, a developmental abnormality with autistic features (Horike et al., 2005); furthermore, alterations in the development of GABAergic neuron circuitry have been found in mice lacking the Methyl-CpG binding protein 2 (MeCP2) gene, whose mutations are responsible for Rett syndrome (Medrihan et al., 2008; Zhang et al., 2010). Lastly, a large number of synaptic-related genes have been implicated in small subsets of patients with ASDs (in total, accounting for probably less than 3–4% of the cases) (Buxbaum, 2009; Radyushkin et al., 2009). Thus, it appears that abnormalities in both the early-determined size and scaffolding of the cerebral cortex and later developing synaptic connections may play a role in individual cases of autism.