ndividuals by analyzing the distribution and clustering of hundreds and PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19817879 thousands of SNPs that have successfully been searched for candidate genes. The first GWAS for ASD was undertaken by Lauritsen et al. in 2006 using 600 DNA markers in an isolated population of affected individuals from the Faroe Islands. They found an association of the chromosome 3p25.3 band, and later, other investigators studied more subjects with larger collections of genotyped markers and found several chromosome bands and regions ascertained when specific SNPs were over-represented in the ASD subjects, including 5p14.1, 5p15 and 16p13p21. The studies implicated several gene families, including the cadherin family, encoding proteins for neuronal cell adhesion, while other genes were implicated in axonal guidance with lower gene expression levels in brain specimens from individuals with ASD, reviewed by Holt and Monaco. Since that time, several additional studies searching for clinically relevant and known genes for ASD have identified a new collection of ASD genes. The ability to identify an increased number of SNPs with advanced genetic platforms and extensive approaches using bioinformatics have led to improved access and a more thorough analysis. This has led to comparing genotyping data from GWAS and DNA copy number variants with the Int. J. Mol. Sci. 2015, 16 6467 identification of structural genetic defects, such as submicroscopic deletions or duplications of the genome, which was not possible a few years ago. Separate studies using array comparative genomic hybridization or microarray analysis to investigate those individuals with ASD continue to yield useful data in identifying candidate genes for ASD in affected individuals. The yield for microarray analysis is reported to be approximately 20% for identifying deletions or duplications at sites where known or candidate ASD genes are present. The use of more advanced technology, such as next-generation sequencing will yield additional valuable information on the location and description of lesions of genes contributing to ASD with increasing evidence for specific and recurring mutations of single genes involved with neurodevelopment and function, leading to potential therapeutic discoveries and interventions. Autism is frequent in single-gene conditions, such as fragile X syndrome, tuberous sclerosis, Rett syndrome or neurofibromatosis, but single-gene disorders as a whole account for less than 20% of all cases; therefore, most individuals with ASD are non-syndromic. The heritability of ASD, which takes into consideration the extent of genetic factors contributing to autism, is estimated to be as high as 90%; hence the relevance and continued importance of investigating the role of genetics in the causation of ASD and expanded diagnostic testing 
to inform and guide treatment for individuals with identifiable genetic disturbances. A current list of clinically relevant and known candidate genes for ASD is needed for diagnostic testing and genetic counselling purposes in the clinical setting. Historically, a previous list of known or candidate genes showing an association with ASD was reported in 2011 by Holt and Monaco with the placement of 175 genes on chromosome ideograms. A much greater number of validated genes are now recognized as playing a pivotal role in ASD, warranting an updated, revised summary. We will utilize high-resolution chromosome Debio-1347 site ideograms to plot the location of genes now recognized by