This is our latest publication in Frontiers (see http://bit.ly/1HmFfnV).  The idea for this study came from the large number of genes currently identified as conferring risk for autism.  In all, these risk genes number in the thousands and account for about one-sixth of our genome. Thus far there has been an insistence from researchers to claim as a unifying characteristic of these genes their putative role in synaptic mechanisms.  We believe this is very naive. Thus in our research we have pursued 2 ideas: 1) The variety of biochemical pathways involved by risk genes suggests that no singular mechanism appears to be affected. If this is the case, it may not be the physiological function of the gene but its physical characteristics that may confer risk, and 2) Genes are used during evolution for different purposes. The more primitive genes had a role in cell division and basic metabolism. From there on the level of complexity increased to confer a cell its ability to move and later on to develop complex specialized functions of which synaptic connections was one of them.  Just to say that the same basic mechanisms involved in forming a synaptic connection had an earlier role in cell division and migration.  It is this earlier mechanism that we believe is affected in autism. A short explanation of the article, written by my wife Emily Casanova, was given in her blog: Our Latest Publication: Genetics studies indicate that neural induction and early neuronal maturation are disturbed in autism.