While these studies generally support a link between reduced SLC1A2 activity and autism pathogenesis, the unexpected lack of correlation between the expression of TGFB genes and SLC1A2 in our study suggests that an unrelated epigenetic silencing of SLC1A2 in autism may disrupt the link between TGFB expression and SLC1A2. This evidence concerns the gene SLC1A2 and autism.