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3. A de novo X;8 translocation creates a PTK2-THOC2 gene fusion with THOC2 expression knockdown in a patient with psychomotor retardation and congenital cerebellar hypoplasia

4. Exome sequencing in children of women with skewed X-inactivation identifies atypical cases and complex phenotypes

5. A New Case of 13q12.2q13.1 Microdeletion Syndrome Contributes to Phenotype Delineation

6. EXOME SEQUENCING REVEALS A NEW CLN5 MUTATION IN AN ADULT FORM OF CEREBELLAR ATAXIA

8. Cover Image, Volume 170A, Number 7, July 2016

9. Whole exome sequencing is necessary to clarify ID/DD cases with de novo copy number variants of uncertain significance: Two proof-of-concept examples

11. A NOVEL GENE FOR SPINOCEREBELLAR ATAXIA (SCA) LINKED TO CHROMOSOME 6 AND INVOLVED IN FATTY ACID METABOLISM

12. A NOVEL GENE FOR SPINOCEREBELLAR ATAXIA (SCA) LINKED TO CHROMOSOME 6 AND FATTY ACID METABOLISM

16. A novel 3q29 deletion associated with autism, intellectual disability, psychiatric disorders, and obesity

17. Two families with novel missense mutations in COL4A1: When diagnosis can be missed

18. Array-Comparative Genomic Hybridization Analysis in Fetuses with Major Congenital Malformations Reveals that 24% of Cases Have Pathogenic Deletions/Duplications

19. Large cryptic genomic rearrangements with apparently normal karyotypes detected by array-CGH

20. ELOVL5 Mutations Cause Spinocerebellar Ataxia 38

21. Bilaterally cleft lip and bilateral thumb polydactyly with triphalangeal component in a patient with twode novodeletions of HSA 4q32 and 4q34 involvingPDGFC,GRIA2, andFBXO8genes

22. Ade novoX;8 translocation creates aPTK2-THOC2gene fusion withTHOC2expression knockdown in a patient with psychomotor retardation and congenital cerebellar hypoplasia

23. Array-Comparative Genomic Hybridization Analysis in Fetuses with Major Congenital Malformations Reveals that 24% of Cases Have Pathogenic Deletions/Duplications.

24. Bilaterally cleft lip and bilateral thumb polydactyly with triphalangeal component in a patient with two De novo deletions of HSA 4q32 and 4q34 involving PDGFC, GRIA 2, and FBXO 8 genes.

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