of unaffected sibs of people with autism. Despite the wide disparities in the sources of the control CNVs, and the potential for different sources of bias, the results converge in pointing to the involvement of the synapse, the PSD, and more specifically, ARC and NMDAR complexes. Finally, and fully independent of those analyses, we show a significant enrichment for genes in the NMDAR complex in a meta-analysis of case–control data sets. We think it likely that the weaker finding for the NMDAR complex in the large case–control study compared with the relatively small de novo study, and the absence of association to ARC in the former, reflects the much lower power of the case–control design as a result of poorer enrichment for pathogenic CNVs.
