The applicability of these pathogenetic mechanisms to the great majority of ASD cases remains unknown. Furthermore, the heterogeneity of phenotypes found when modeling these mutations in animals and the inherent difficulty in creating behavioral phenotypes of ASD in rodents have complicated the construction of credible animal models of ASD. It is possible that the heterogeneity of rare mutations found in ASD, as currently conceptualized, denies a unified understanding of the pathophysiology of the disorder. However, emerging evidence suggests that current genomic data, when considered in the framework of gene network analyses, point to a common pathophysiological substrate in ASD rooted in the embryonic development of the cerebral cortex (Parikshak et al., 2013; Willsey et al., 2013).
