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Further analysis by high\u2010density oligonucleotide microarray was performed, showing an 8.8\u2010Mb heterozygous deletion at 21q21.1\u2013q21.3. Interestingly, the deletion is distal to the translocation breakpoint on chromosome 21. The deletion involves 19 genes, including <jats:italic>NCAM2<\/jats:italic> and <jats:italic>GRIK1<\/jats:italic>, both of which are associated with normal brain development and function, and have been considered as possible candidate genes in autism and other neurobehavioral disorders. This case underscores the utility of genomewide microarray analysis for the detection of copy number alterations in patients with apparently balanced complex rearrangements and abnormal phenotypes. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajmg.a.33176","type":"journal-article","created":{"date-parts":[[2009,12,23]],"date-time":"2009-12-23T20:35:06Z","timestamp":1261600506000},"page":"196-202","source":"Crossref","is-referenced-by-count":30,"title":["A de novo 8.8\u2010Mb deletion of 21q21.1\u2013q21.3 in an autistic male with a complex rearrangement involving chromosomes 6, 10, and 21"],"prefix":"10.1002","volume":"152A","author":[{"given":"Chad R.","family":"Haldeman\u2010Englert","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kimberly 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