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Background There is growing evidence that common diseases might not result from af ew common variants, but rather from many rare variants across many genes/loci. This is likely to be particularly true for disorders such as autism where the fecundity of affected individuals is exceptionally low (~5%) and thus disease-predisposing alleles are unlikely to be transmitted. Since these different disease-contributing genes give rise to a shared disease phenotype, it is likely that their protein products contribute to shared biological processes, such as particular protein pathways or cellular networks. Identifying the common network(s) among these genes would allow the screening of a small subset of genes for early diagnosis and these networks could present multiple points for early intervention. Methods

Candidate genes and biological processes in de novo CNVs from autistic individuals