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Congenital Deafness with Labyrinthine Aplasia, Microtia, and Microdontia

Synonyms: Congenital Deafness with Inner Ear Agenesis, Microtia, and Microdontia; LAMM Syndrome
, MS
Dr John T Macdonald Foundation
Department of Human Genetics
John P Hussman Institute for Human Genomics
Miami, Florida
, MD
Dr John T Macdonald Foundation
Department of Human Genetics
John P Hussman Institute for Human Genomics
Miami, Florida

Initial Posting: .


Clinical characteristics

Congenital deafness with labyrinthine aplasia, microtia, and microdontia (LAMM syndrome) is characterized by: profound bilateral congenital sensorineural deafness associated with inner ear anomalies (most often bilateral complete labyrinthine aplasia); microtia (type I) that is typically bilateral (although unilateral microtia and normal external ears are observed on occasion); and microdontia (small teeth). Individuals with LAMM syndrome commonly have motor delays during infancy presumably due to impaired balance from inner ear (vestibular) abnormalities. Growth, physical development, and cognition are normal.


Diagnosis, which is based on clinical findings, can be confirmed by molecular genetic testing of FGF3, the only gene in which pathogenic variants are known to cause LAMM syndrome.


Treatment of manifestations: Enrollment in appropriate early intervention programs and educational programs for the hearing-impaired; consideration of vibrotactile hearing devices or brainstem implants for individuals with complete labyrinth aplasia; consideration of cochlear implantation for those with a cochleovestibular nerve and a cochlear remnant; routine ophthalmologic management of strabismus.

Prevention of secondary complications: Attention to the increased risk for accidents secondary to delayed gross development and deafness.

Surveillance: Yearly evaluations with a physician familiar with LAMM syndrome or other forms of hereditary deafness; regular ENT and dental evaluations.

Agents/circumstances to avoid: Patients with residual cochlear function should avoid noise exposure. Because of the high risk for disorientation when submerged in water, swimming needs to be undertaken with caution.

Evaluation of relatives at risk: It is recommended that sibs have hearing screening to allow early diagnosis and treatment of hearing impairment.

Genetic counseling

LAMM syndrome is inherited in an autosomal recessive manner. At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being a non-carrier. Carrier testing for at-risk family members is possible if the pathogenic variants in the family have been identified. If the pathogenic variants have been identified in an affected family member, prenatal testing for at-risk pregnancies is possible through laboratories offering either prenatal testing for the gene of interest or custom testing.


Clinical Diagnosis

The diagnosis of congenital deafness with labyrinthine aplasia, microtia, and microdontia (LAMM syndrome) is suspected in individuals with the following:

  • Profound congenital sensorineural deafness
  • Severe inner ear anomalies diagnosed by a CT scan or MRI of the inner ear. The most common inner ear anomaly is complete labyrinthine aplasia with no recognizable structure in the inner ear (also referred to as Michel aplasia). (Figure 1C)
  • Microtia with shortening of the upper part of the auricles (also referred to as type I microtia) (Figure 1A)
  • Microdontia (small sized teeth) with widely spaced teeth (Figure 1B)
Figure 1.

Figure 1.

Congenital deafness with labyrinthine aplasia, microtia, and microdontia

Some individuals may also show gross motor developmental delay during infancy (presumably due to the absence of vestibular system) accompanied by additional features that include:

  • Hypoplasia/dysplasia of middle ear anatomic structures identified by imaging studies
  • Stenosis of the jugular foramen with enlarged emissary vein identified by imaging studies

Molecular Genetic Testing

Gene. FGF3 is the only gene in which pathogenic variants are known to cause congenital deafness with labyrinthine aplasia, microtia, and microdontia.

Table 1.

Molecular Genetic Testing Used in Congenital Deafness with Labyrinthine Aplasia, Microtia, and Microdontia

Gene 1Test MethodVariants Detected 2Variant Detection Frequency by Test Method 3
FGF3Sequence analysis 4Sequence variants13/13 unrelated families 5
Deletion/duplication analysis 6Exon or whole-gene deletionsUnknown, none reported 7

See Molecular Genetics for information on allelic variants.


The ability of the test method used to detect a variant that is present in the indicated gene


Sequence analysis detects variants that are benign, likely benign, of uncertain significance, likely pathogenic, or pathogenic. Pathogenic variants may include small intragenic deletions/insertions and missense, nonsense, and splice site variants; typically, exon or whole-gene deletions/duplications are not detected. For issues to consider in interpretation of sequence analysis results, click here.


Testing that identifies exon or whole-gene deletions/duplications not readily detectable by sequence analysis of the coding and flanking intronic regions of genomic DNA; included in the variety of methods that may be used are: quantitative PCR, long-range PCR, multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray (CMA) that includes this gene/chromosome segment.


Although no large deletions/duplications have been reported in FGF3, such testing would be expected to detect (multi)exon and whole-gene deletions/duplications.

Testing Strategy

Confirmation of the diagnosis in a proband. In an individual with characteristic clinical findings, identification of a deleterious FGF3 variant by molecular genetic testing confirms the diagnosis of LAMM syndrome.

Carrier testing for at-risk relatives requires prior identification of the pathogenic variants in the family.

Note: Carriers are heterozygotes for this autosomal recessive disorder and are not at risk of developing the disorder.

Prenatal diagnosis and preimplantation genetic diagnosis (PGD) for at-risk pregnancies require prior identification of the pathogenic variants in the family.

Clinical Characteristics

Clinical Description

Labyrinthine aplasia, microtia, and microdontia (LAMM syndrome) was originally described by Tekin et al [2007]. Since then 56 individuals with homozygous and compound heterozygous FGF3 pathogenic variants from 13 consanguineous and non-consanguineous families have been reported [Sensi et al 2011]. Age at diagnosis ranges from one month to 50 years.

Profound congenital sensorineural deafness is bilateral in all individuals reported to date. Most have bilateral complete labyrinthine aplasia, some have unilateral complete labyrinth aplasia and visible but severely malformed inner ear structures in the other ear, and a few have some inner ear structure present bilaterally [Tekin et al 2007, Ramsebner et al 2010, Riazuddin et al 2011].

Type I microtia with shortening of auricles above the crura of the antihelix tends to be bilateral in most. Unilateral microtia and bilateral normal external ears have been reported in individuals with the p.Arg95Trp pathogenic variant. Anteverted ears and large skin tags or lobulation of the upper side of the auricle can be seen in some [Tekin et al 2008].

Small teeth have been observed in all reported individuals. Dental anomalies include conical shape and decreased tooth diameter resulting in widely spaced teeth. Loss of tooth height and peg-shaped lateral incisors have been seen. Supernumerary upper lateral incisors and absence of the first premolars have been observed.

Mild micrognathia and excessive caries were noted in one adult.

Hypodontia or dental root anomalies have not been observed [Tekin et al 2007].


  • Motor delays during infancy, presumably the result of impaired balance; commonly seen
  • Stenosis of the jugular foramen with enlarged emissary vein diagnosed by cranial imaging with no clinical manifestations
  • Normal growth and physical development are normal
  • Average or above average cognition; affected individuals often attend and thrive at schools for the hearing impaired.
  • Absence of limb anomalies and lacrimal findings (seen in some FGFR-related syndromes)

Findings that may be incidental or part of the LAMM syndrome spectrum include: hypoplastic alae nasi, mild anatomic defects including unilateral stenosis of the uretero-pelvic junction, ocular abnormalities such as strabismus-hypermetropia, and mildly distinctive facial features such as long facies, downslanting palpebral fissures, deep-set eyes, high nasal bridge, and mild micrognathia.

Life span is not typically altered in individuals with classic LAMM syndrome. Healthy adults reaching their 40s and 50s have been reported [Tekin et al 2007, Alsmadi et al 2009].

Genotype-Phenotype Correlations

Intra- and interfamilial variability of the clinical phenotype is currently minimal in LAMM syndrome, except for those individuals with the c.283C>T (p.Arg95Trp) pathogenic variant (see Molecular Genetics); p.Arg95Trp is associated with a less severe phenotype than the other FGF3 pathogenic variants [Ramsebner et al 2010, Riazuddin et al 2011].

  • Microtia was not observed in eight of 11 individuals homozygous for p.Arg95Trp; in contrast none of the persons reported with other pathogenic variants had normal-appearing external ears.
  • Inner ear structures were identified in seven of 20 individuals homozygous for p.Arg95Trp; in contrast, persons reported with other pathogenic variants had either no inner ear components or primitive vesicle-like structures.


Congenital deafness with labyrinthine aplasia, microtia, and microdontia (LAMM syndrome) has also been described as congenital deafness with inner ear agenesis, microtia, and microdontia.


LAMM syndrome is very rare; no prevalence estimates have been established. It has been reported in 56 individuals from 13 unrelated families.

Differential Diagnosis

LADD (lacrimo-auriculo-dento-digital) syndrome is a multiple congenital anomaly syndrome characterized by aplasia, atresia, or hypoplasia of the lacrimal and salivary systems; cup-shaped ears; hearing loss; and dental and digital (particularly thumb) anomalies. Pathogenic variants in FGFR2, FGF10, and FGFR3 have been associated with this syndrome. Inheritance is autosomal dominant.

Other single-gene disorders or microdeletion/microduplication syndromes should be considered in individuals with intellectual disability in addition to typical anomalies seen in LAMM syndrome [Dill et al 2011].


Evaluations Following Initial Diagnosis

To establish the extent of disease and needs in an individual diagnosed with congenital deafness with labyrinthine aplasia, microtia, and microdontia (LAMM syndrome), the following evaluations are recommended:

  • ENT evaluation with CT/MRI of the temporal bones to evaluate inner ear anomalies that may influence habilitation options (see Treatment of Manifestations)
  • Audiology evaluation
  • Dental evaluation
  • Renal ultrasound examination to evaluate for kidney anomalies, including unilateral stenosis of the uretero-pelvic junction
  • Ophthalmology evaluation for strabismus and hypermetropia
  • Consultation with a clinical geneticist and/or genetic counselor

Treatment of Manifestations

Ideally, the team evaluating and treating a deaf individual should include an otolaryngologist with expertise in the management of early childhood otologic disorders, an audiologist experienced in the assessment of hearing loss in children, a clinical geneticist, and a pediatrician. The expertise of an educator of the Deaf, a neurologist, and a pediatric ophthalmologist may also be required.

  • Enrollment in appropriate early intervention programs and educational programs for the hearing-impaired
  • An important part of the evaluation is determining the appropriate habilitation option. Possibilities include hearing aids, vibrotactile devices, brain stem implants, and cochlear implantation:
    • Consideration of vibrotactile hearing devices or brain stem implants for individuals with complete labyrinth aplasia [Riazuddin et al 2011]
    • Evaluation for cochlear implantation in those individuals with a cochleovestibular nerve and a cochlear remnant. Cochlear implantation can be considered in children over age 12 months with severe-to-profound hearing loss.
  • Routine ophthalmologic management of strabismus, if present

Prevention of Secondary Complications

Regardless of its etiology, uncorrected hearing loss has consistent sequelae: Auditory deprivation through age two years is associated with poor reading performance, poor communication skills, and poor speech production. Educational intervention is insufficient to completely remediate these deficiencies.

In contrast, early auditory intervention (whether through amplification or cochlear implantation) is effective (see Deafness and Hereditary Hearing Loss Overview). However, the presence of severe inner ear anomalies and Michel aplasia in individuals with LAMM syndrome limits auditory habilitation options.

Delayed gross development (presumably the result of impaired balance and profound deafness) increases the risk for accidents and trauma.

  • The risk for accidents can be addressed in part by use of visual or vibrotactile alarm systems in homes and schools.
  • The risk for pedestrian injury can be reduced by choosing routes with visual displays of crosswalks.
  • Anticipatory education of parents, health providers, and educational programs about hazards can help address the risk for falls [Gaebler-Spira & Thornton 2002, Chakravarthy et al 2007].


Yearly evaluations by the multidisciplinary team mentioned in Treatment of Manifestations is appropriate.

Agents/Circumstances to Avoid

Noise exposure is a well-recognized environmental cause of hearing loss. Since this risk can be minimized by avoidance, individuals with LAMM syndrome and a residual cochlea should be counseled appropriately.

Because of the high risk for disorientation when submerged in water, swimming needs to be undertaken with caution.

Evaluation of Relatives at Risk

Since some individuals with LAMM syndrome can have normal-appearing ears, an audiology evaluation is recommended for sibs at 25% risk to allow early diagnosis and treatment of hearing impairment.

See Genetic Counseling for issues related to testing of at-risk relatives for genetic counseling purposes.

Therapies Under Investigation

Search for access to information on clinical studies for a wide range of diseases and conditions. Note: There may not be clinical trials for this disorder.

Genetic Counseling

Genetic counseling is the process of providing individuals and families with information on the nature, inheritance, and implications of genetic disorders to help them make informed medical and personal decisions. The following section deals with genetic risk assessment and the use of family history and genetic testing to clarify genetic status for family members. This section is not meant to address all personal, cultural, or ethical issues that individuals may face or to substitute for consultation with a genetics professional. —ED.

Mode of Inheritance

Congenital deafness with labyrinthine aplasia, microtia, and microdontia (LAMM syndrome) is inherited in an autosomal recessive manner.

Risk to Family Members

Parents of a proband

  • The parents of an affected child are obligate heterozygotes (i.e., carriers of one mutated allele).
  • Heterozygotes (carriers) are asymptomatic.

Sibs of a proband

  • At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being a non-carrier.
  • Once an at-risk sib is known to be unaffected, the risk of his/her being a carrier is 2/3.
  • Heterozygotes (carriers) are asymptomatic.

Offspring of a proband. Unless an individual with LAMM syndrome has children with an affected individual or a carrier, his/her offspring will be obligate heterozygotes (carriers) for a pathogenic variant in FGF3.

Other family members. Each sib of the proband’s parents is at a 50% risk of being a carrier.

Carrier (Heterozygote) Detection

Carrier testing for at-risk family members is possible if the pathogenic variants in the family have been identified.

Related Genetic Counseling Issues

See Management, Evaluation of Relatives at Risk for information on evaluating at-risk relatives for the purpose of early diagnosis and treatment.

Family planning

  • The optimal time for determination of genetic risk, clarification of carrier status, and discussion of the availability of prenatal testing is before pregnancy.
  • It is appropriate to offer genetic counseling (including discussion of potential risks to offspring and reproductive options) to young adults who are affected, are carriers, or are at risk of being carriers.

DNA banking is the storage of DNA (typically extracted from white blood cells) for possible future use. Because it is likely that testing methodology and our understanding of genes, allelic variants, and diseases will improve in the future, consideration should be given to banking DNA of affected individuals.

Prenatal Testing and Preimplantation Genetic Diagnosis

Once the pathogenic variants have been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic diagnosis are possible.

Differences in perspective may exist among medical professionals and within families regarding the use of prenatal testing, particularly if the testing is being considered for the purpose of pregnancy termination rather than early diagnosis. While most centers would consider decisions regarding prenatal testing to be the choice of the parents, discussion of these issues is appropriate.


GeneReviews staff has selected the following disease-specific and/or umbrella support organizations and/or registries for the benefit of individuals with this disorder and their families. GeneReviews is not responsible for the information provided by other organizations. For information on selection criteria, click here.

  • American Society for Deaf Children (ASDC)
    800 Florida Avenue Northeast
    Suite 2047
    Washington DC 20002-3695
    Phone: 800-942-2732 (Toll-free Parent Hotline); 866-895-4206 (toll free voice/TTY)
    Fax: 410-795-0965
    This site, developed with support from the National Institute on Deafness and Other Communication Disorders, provides information about newborn hearing screening and hearing loss.
  • Children's Craniofacial Association (CCA)
    13140 Coit Road
    Suite 517
    Dallas TX 75240
    Phone: 800-535-3643 (toll-free)
  • National Association of the Deaf (NAD)
    8630 Fenton Street
    Suite 820
    Silver Spring MD 20910
    Phone: 301-587-1788; 301-587-1789 (TTY)
    Fax: 301-587-1791

Molecular Genetics

Information in the Molecular Genetics and OMIM tables may differ from that elsewhere in the GeneReview: tables may contain more recent information. —ED.

Table A.

Congenital Deafness with Labyrinthine Aplasia, Microtia, and Microdontia: Genes and Databases

GeneChromosome LocusProteinLocus-Specific DatabasesHGMDClinVar
FGF311q13​.3Fibroblast growth factor 3FGF3 databaseFGF3FGF3

Data are compiled from the following standard references: gene from HGNC; chromosome locus from OMIM; protein from UniProt. For a description of databases (Locus Specific, HGMD, ClinVar) to which links are provided, click here.

Table B.

OMIM Entries for Congenital Deafness with Labyrinthine Aplasia, Microtia, and Microdontia (View All in OMIM)


Gene structure. The normal full-length cDNA is encoded in three exons spanning 9.4 kb (9457 bp) of the genomic DNA. The cDNA comprises 1548 bp with an open reading frame of 720 nucleotides encoding 239 amino acids. For a detailed summary of gene and protein information, see Table A, Gene.

Pathogenic variants. Twelve FGF3 pathogenic variants have been described in LAMM syndrome. Six are missense variants and six are nonsense variants or small deletions. Most are private variants except for p.Arg104Ter, which has been observed in Turkish, Pakistani, and Italian families [Ramsebner et al 2010, Riazuddin et al 2011, Sensi et al 2011].

Table 2.

Selected FGF3 Pathogenic Variants

DNA Nucleotide ChangePredicted Protein ChangeReference Sequences

Note on variant classification: Variants listed in the table have been provided by the authors. GeneReviews staff have not independently verified the classification of variants.

Note on nomenclature: GeneReviews follows the standard naming conventions of the Human Genome Variation Society (varnomen​ See Quick Reference for an explanation of nomenclature.

Normal gene product. Fibroblast growth factor proteins function in embryonic development, cell growth, morphogenesis, tissue repair, and tumor growth and invasion [Pownall & Isaacs 2010]. They mainly function through three pathways including the RAS/MAP kinase pathway (the main pathway), phosphoinositides 3 kinase/AKT pathway, and the phospholipase C gamma pathway.

Physiologically, FGF3 binds to the FGFR (fibroblast growth factor receptor) 1b and 2b to activate its signaling cascade, thus regulating cellular proliferation, survival, migration, and differentiation [Zelarayan et al 2007]. A unique feature of FGFs is that they act in concert with heparin or heparin sulfate proteoglycans to activate the signaling cascade and induce a variety of cellular processes. Along with FGF8 and FGF10, FGF3 plays a crucial role in the embryonic development of the otic placode (which forms the inner ear) and its eventual differentiation into the vestibular and cochlear structures [Vendrell et al 2000, Wright & Mansour 2003, Toriello et al 2004]. Studies in mice and zebrafish have also shown the role of FGF3 in dental morphogenesis [Kettunen et al 2000, Jackman et al 2004].

Abnormal gene product. Pathogenic variants reported are mainly nonsense and frameshift (leading to truncated proteins), null variants (absence of protein from nonsense-mediated mRNA decay), or missense variants in highly conserved amino acid residues (probably resulting in greatly reduced or absent protein). Molecular modeling suggests that the p.Arg95Trp pathogenic variant does not impair the interaction of FGF3 with FGFR2b receptors or heparin sulfate binding sites, which may result in residual function of FGF3 [Riazuddin et al 2011].


Literature Cited

  • Alsmadi O, Meyer BF, Alkuraya F, Wakil S, Alkayal F, Al-Saud H, Ramzan K, Al-Sayed M. Syndromic congenital sensorineural deafness, microtia and microdontia resulting from a novel homoallelic mutation in fibroblast growth factor 3 (FGF3). Eur J Hum Genet. 2009;17:14–21. [PMC free article: PMC2985964] [PubMed: 18701883]
  • Chakravarthy B, Vaca FE, Lotfipour S, Bradley D. Pediatric pedestrian injuries: emergency care considerations. Pediatr Emerg Care. 2007;23:738–44. [PubMed: 18090111]
  • Dill P, Schneider J, Weber P, Trachsel D, Tekin M, Jakobs C, Thöny B, Blau N. Pyridoxal phosphate-responsive seizures in a patient with cerebral folate deficiency (CFD) and congenital deafness with labyrinthine aplasia, microtia and microdontia (LAMM). Mol Genet Metab. 2011;104:362–8. [PubMed: 21752681]
  • Gaebler-Spira D, Thornton LS. Injury prevention for children with disabilities. Phys Med Rehabil Clin N Am. 2002;13:891–906. [PubMed: 12465566]
  • Gregory-Evans CY, Moosajee M, Hodges MD, Mackay DS, Game L, Vargesson N, Bloch-Zupan A, Rüschendorf F, Santos-Pinto L, Wackens G, Gregory-Evans K. SNP genome scanning localizes oto-dental syndrome to chromosome 11q13 and microdeletions at this locus implicate FGF3 in dental and inner-ear disease and FADD in ocular coloboma. Hum Mol Genet. 2007;16:2482–93. [PubMed: 17656375]
  • Jackman WR, Draper B, Stock D. Fgf signaling is required for zebrafish tooth development. Dev Biol. 2004;274:139–57. [PubMed: 15355794]
  • Kettunen P, Laurikkala J, Itäranta P, Vainio S, Itoh N, Thesleff I. Associations of FGF-3 and FGF-10 with signaling networks regulating tooth morphogenesis. Dev Dyn. 2000;219:322–32. [PubMed: 11066089]
  • Pownall ME, Isaacs HV. FGF Signalling in Vertebrate Development. San Rafael, CA: Morgan & Claypool Life Sciences; 2010.
  • Ramsebner R, Ludwig M, Parzefall T, Lucas T, Baumgartner WD, Bodamer O, Cengiz FB, Schoefer C, Tekin M, Frei K. A. FGF3 mutation associated with differential inner ear malformation, microtia, and microdontia. Laryngoscope. 2010;120:359–64. [PubMed: 19950373]
  • Riazuddin S, Ahmed ZM, Hegde RS, Khan SN, Nasir I, Shaukat U, Riazuddin S, Butman JA, Griffith AJ, Friedman TB, Choi BY. Variable expressivity of FGF3 mutations associated with deafness and LAMM syndrome. BMC Med Genet. 2011;12:21. [PMC free article: PMC3042908] [PubMed: 21306635]
  • Sensi A, Ceruti S, Trevisi P, Gualandi F, Busi M, Donati I, Neri M, Ferlini A, Martini A. LAMM syndrome with middle ear dysplasia associated with compound heterozygosity for FGF3 mutations. Am J Med Genet. A. 2011;155A:1096–101. [PubMed: 21480479]
  • Tekin M, Hişmi BO, Fitoz S, Ozdağ H, Cengiz FB, Sirmaci A, Aslan I, Inceoğlu B. EYüksel-Konuk EB, Yilmaz ST, Yasun O, Akar N. Homozygous mutations in fibroblast growth factor 3 are associated with a new form of syndromic deafness characterized by inner ear agenesis, microtia, and microdontia. Am J Hum Genet. 2007;80:338–44. [PMC free article: PMC1785350] [PubMed: 17236138]
  • Tekin M, Oztürkmen Akay H, Fitoz S, Birnbaum S, Cengiz FB, Sennaroğlu L, Incesulu A, Yüksel Konuk EB, Hasanefendioğlu Bayrak A, Sentürk S, Cebeci I, Utine GE, Tunçbilek E, Nance WE, Duman D. Homozygous FGF3 mutations result in congenital deafness with inner ear agenesis, microtia, and microdontia. Clin Genet. 2008;73:554–65. [PubMed: 18435799]
  • Toriello HV, Reardon W, Gorlin RJ. Hereditary Hearing Loss and Its Syndromes. 2 ed. New York, NY: Oxford University Press; 2004.
  • Vendrell V, Carnicero E, Giraldez F, Alonso MT, Schimmang T. Induction of inner ear fate by FGF3. Development. 2000;127:2011–9. [PubMed: 10769226]
  • Wright TJ, Mansour SL. FGF3 and Fgf10 are required for mouse otic placode induction. Development. 2003;130:3379–90. [PubMed: 12810586]
  • Zelarayan LC, Vendrell V, Alvarez Y, Domínguez-Frutos E, Theil T, Alonso MT, Maconochie M, Schimmang T. Differential requirements for FGF3, FGF8 and FGF10 during inner ear development. Dev Biol. 2007;308:379–91. [PubMed: 17601531]

Chapter Notes


This work was supported by NIH-NIDCD grant R01DC009645 to M.T.

Author Notes

John P Hussman Institute for Human Genomics: Genetic Studies of Deafness

Division of Clinical and Translation Genetics: Deafness Clinic

Revision History

  • 20 September 2012 (me) Review posted live
  • 9 June 2012 (mt) Original submission
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