The Autism Genome Project Consortium conducted a large-scale genetic linkage and chromosomal rearrangement study to identify autism risk loci. Using Affymetrix 10K SNP arrays and 1,181 families with at least two affected individuals, they performed the largest linkage scan to date and analyzed copy number variations (CNVs) in these families. The study identified chromosome 11p12–p13 and neurexins as candidate loci for autism risk. Neurexins, which are involved in glutamatergic synaptogenesis, were found to team with previously implicated neuroligins, highlighting glutamate-related genes as promising candidates for contributing to autism. The study also explored the effects of removing families with CNVs, which amplified linkage signals in specific regions, particularly 11p12–p13 and 15q23–25.3. The findings suggest that CNVs play a significant role in autism risk and highlight the importance of fine-mapping and further genetic studies in these regions.The Autism Genome Project Consortium conducted a large-scale genetic linkage and chromosomal rearrangement study to identify autism risk loci. Using Affymetrix 10K SNP arrays and 1,181 families with at least two affected individuals, they performed the largest linkage scan to date and analyzed copy number variations (CNVs) in these families. The study identified chromosome 11p12–p13 and neurexins as candidate loci for autism risk. Neurexins, which are involved in glutamatergic synaptogenesis, were found to team with previously implicated neuroligins, highlighting glutamate-related genes as promising candidates for contributing to autism. The study also explored the effects of removing families with CNVs, which amplified linkage signals in specific regions, particularly 11p12–p13 and 15q23–25.3. The findings suggest that CNVs play a significant role in autism risk and highlight the importance of fine-mapping and further genetic studies in these regions.