Human Gene Module / Chromosome 11 / KMT2A

KMT2ALysine (K)-specific methyltransferase 2A

Score
1S
High Confidence, Syndromic Criteria 1.1, Syndromic
Autism Reports / Total Reports
5 / 20
Rare Variants / Common Variants
89 / 0
Aliases
KMT2A, hCG_1732268,  ALL-1,  CXXC7,  HRX,  HTRX1,  MLL,  MLL/GAS7,  MLL1,  MLL1A,  TET1-MLL,  TRX1,  WDSTS
Associated Syndromes
Wiedemann-Steiner syndrome
Genetic Category
Rare Single Gene Mutation, Syndromic
Chromosome Band
11q23.3
Associated Disorders
EPS, EP, ID, ASD, ADHD, DD/NDD
Relevance to Autism

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in Jones et al., 2012 (PMID 22795537). Two additional de novo LoF variants in KMT2A were identified in ASD probands from the ASD: Genomes to Outcome Study cohort in Yuen et al., 2017 (PMID 28263302). Based on multiple de novo LoF variants in this gene, a probability of LoF intolerance rate (pLI) > 0.9, and higher-than-expected mutation rate (false discovery rate < 15%), KMT2A was determined to be an ASD candidate gene in Yuen et al., 2017. Mutations in this gene have also been identified in additional individuals presenting with developmental delay/intellectual disability (PMIDs 25533962, 27479843, 27848944)

Molecular Function

This gene encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis via its histone H3 lysine 4 (H3K4) methyltransferase activity, which mediates chromatin modifications associated with epigenetic transcriptional activation. Mutations in this gene are associated with Wiedemann-Steiner syndrome (OMIM:605130), a syndrome characterized by hairy elbows (hypertrichosis cubiti), intellectual disability, a distinctive facial appearance, and short stature.

Reports related to KMT2A (20 Reports)
# Type Title Author, Year Autism Report Associated Disorders
1 Support De novo mutations in MLL cause Wiedemann-Steiner syndrome. Jones WD , et al. (2012) No DD, ID, ASD
2 Primary Synaptic, transcriptional and chromatin genes disrupted in autism. De Rubeis S , et al. (2014) Yes -
3 Support The contribution of de novo coding mutations to autism spectrum disorder. Iossifov I , et al. (2014) Yes -
4 Recent Recommendation Large-scale discovery of novel genetic causes of developmental disorders. Deciphering Developmental Disorders Study (2014) Yes -
5 Support Delineation of clinical features in Wiedemann-Steiner syndrome caused by KMT2A mutations. Miyake N , et al. (2015) No DD, ID
6 Recent Recommendation Low load for disruptive mutations in autism genes and their biased transmission. Iossifov I , et al. (2015) Yes -
7 Support Whole exome sequencing reveals a MLL de novo mutation associated with mild developmental delay and without 'hairy elbows': expanding the phenotype ... Steel D , et al. (2015) No DD
8 Support Congenital immunodeficiency in an individual with Wiedemann-Steiner syndrome due to a novel missense mutation in KMT2A. Stellacci E , et al. (2016) No Epilepsy/seizures, microcephaly, DD, ID
9 Support Meta-analysis of 2,104 trios provides support for 10 new genes for intellectual disability. Lelieveld SH , et al. (2016) No -
10 Support High diagnostic yield of syndromic intellectual disability by targeted next-generation sequencing. Martnez F , et al. (2016) No ID
11 Support Clinical exome sequencing: results from 2819 samples reflecting 1000 families. Trujillano D , et al. (2016) No DD, ID
12 Support Whole genome sequencing resource identifies 18 new candidate genes for autism spectrum disorder. C Yuen RK , et al. (2017) Yes -
13 Support Contribution of rare inherited and de novo variants in 2,871 congenital heart disease probands. Jin SC , et al. (2017) No Neurodevelopmental disorders (NDD)
14 Support Exome Pool-Seq in neurodevelopmental disorders. Popp B , et al. (2017) No -
15 Support Molecular and cellular issues of KMT2A variants involved in Wiedemann-Steiner syndrome. Lebrun N , et al. (2017) No ID, hypotonia, stereotypies
16 Recent Recommendation Wiedemann-Steiner syndrome as a major cause of syndromic intellectual disability: A study of 33 French cases. Baer S , et al. (2018) No ASD
17 Support Description of the molecular and phenotypic spectrum of Wiedemann-Steiner syndrome in Chinese patients. Li N , et al. (2018) No -
18 Support A novel deletion mutation in KMT2A identified in a child with ID/DD and blood eosinophilia. Zhang H , et al. (2019) No Stereotypies
19 Support Elucidation of the phenotypic spectrum and genetic landscape in primary and secondary microcephaly. Boonsawat P , et al. (2019) No DD
20 Recent Recommendation Expanding the neurodevelopmental phenotypes of individuals with de novo KMT2A variants. Chan AJS , et al. (2019) No ASD, ID, ADHD
Rare Variants   (89)
Status Allele Change Residue Change Variant Type Inheritance Pattern Parental Transmission Family Type PubMed ID Author, Year
c.901C>T p.Arg301Ter stop_gained De novo - - 30305169 Li N , et al. (2018)
c.269C>A p.Ser90Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.5871T>A p.Tyr1957Ter stop_gained De novo - - 30305169 Li N , et al. (2018)
c.478C>T p.Arg160Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.10837C>T p.Gln3613Ter stop_gained Unknown - - 30305169 Li N , et al. (2018)
c.3241C> T p.Arg1081Ter stop_gained De novo - - 30305169 Li N , et al. (2018)
c.10900+2T>C p.? splice_site_variant De novo - - 30305169 Li N , et al. (2018)
c.3301C>T p.Arg1101Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.4897C>T p.Arg1633Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.6487C>T p.Arg2163Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.7438C>T p.Arg2480Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.7630G>T p.Glu2544Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
c.7975C>T p.Arg2659Ter stop_gained De novo - - 29574747 Baer S , et al. (2018)
delA p.Arg1927fs frameshift_variant De novo - - 28991257 Jin SC , et al. (2017)
c.3334+1G>A p.? splice_site_variant De novo - - 29158550 Popp B , et al. (2017)
c.4696+1G>A p.? splice_site_variant De novo - - 29574747 Baer S , et al. (2018)
c.4897C>T p.Arg1633Ter stop_gained De novo - - 26690532 Steel D , et al. (2015)
c.6781C>T p.Gln2261Ter stop_gained De novo - - 25810209 Miyake N , et al. (2015)
c.7438C>T p.Arg2480Ter stop_gained De novo - - 25810209 Miyake N , et al. (2015)
c.8095C>T p.Arg2699Ter stop_gained De novo - - 31044088 Chan AJS , et al. (2019)
del(G) - frameshift_variant De novo - Simplex 25363768 Iossifov I , et al. (2014)
c.11716C>T p.Arg3906Cys missense_variant De novo - - 30305169 Li N , et al. (2018)
c.3503G> A p.Gly1168Asp missense_variant De novo - - 30305169 Li N , et al. (2018)
c.2618G>T p.Ser873Asn missense_variant De novo - - 29574747 Baer S , et al. (2018)
del(C) - frameshift_variant De novo - Simplex 25363760 De Rubeis S , et al. (2014)
c.3460C>T p.Arg1154Trp missense_variant De novo - - 29574747 Baer S , et al. (2018)
c.3464G>A p.Cys1155Tyr missense_variant De novo - - 29574747 Baer S , et al. (2018)
c.3542G>A p.Gly1181Asp missense_variant De novo - - 29574747 Baer S , et al. (2018)
c.5873A>G p.His1958Arg missense_variant De novo - - 29574747 Baer S , et al. (2018)
c.6080G>A p.Gly2027Glu missense_variant De novo - - 29574747 Baer S , et al. (2018)
c.838C>A p.Pro280Thr missense_variant Unknown - - 25810209 Miyake N , et al. (2015)
c.3566G>A p.Cys1189Tyr missense_variant De novo - - 25810209 Miyake N , et al. (2015)
c.3460C>T p.Arg1154Trp missense_variant De novo - - 29203834 Lebrun N , et al. (2017)
c.3581G>A p.Cys1194Tyr missense_variant De novo - - 29203834 Lebrun N , et al. (2017)
c.8558T>G p.Met2853Arg missense_variant De novo - - 29203834 Lebrun N , et al. (2017)
c.8543T>C p.Leu2848Pro missense_variant De novo - - 31044088 Chan AJS , et al. (2019)
c.10780C>T p.Gln3594Ter stop_gained De novo - - 27848944 Trujillano D , et al. (2016)
c.6052delG p.Glu2018fsTer7 frameshift_variant De novo - - 30305169 Li N , et al. (2018)
c.7144C>T p.Arg2382Ter stop_gained De novo - Simplex 22795537 Jones WD , et al. (2012)
c.2944T>A p.Ser982Thr missense_variant De novo - - 25363760 De Rubeis S , et al. (2014)
c.3481T>G p.Cys1161Gly missense_variant De novo - - 27320412 Stellacci E , et al. (2016)
c.2510dupC p.Trp838llefsTer9 frameshift_variant De novo - - 30305169 Li N , et al. (2018)
c.8531G>T p.Cys2844Phe missense_variant De novo - - 27479843 Lelieveld SH , et al. (2016)
c.2461dup p.Ser821fs frameshift_variant De novo - - 27479843 Lelieveld SH , et al. (2016)
c.2318dupC p.Ser774ValfsTer12 frameshift_variant De novo - - 30305169 Li N , et al. (2018)
c.4059delC p.Pro1354LeufsTer2 frameshift_variant De novo - - 30305169 Li N , et al. (2018)
c.1142dup p.Ala383GlyfsTer6 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.3837delT p.Pro1281LeufsTer75 frameshift_variant De novo - - 30305169 Li N , et al. (2018)
c.10752dupA p.Gly3585ArgfsTer8 frameshift_variant De novo - - 30305169 Li N , et al. (2018)
c.2318dup p.Ser774ValfsTer12 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.5603del p.Pro1868GlnfsTer3 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.8270dup p.Ile2758AspfsTer2 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.5251A>T p.Lys1751Ter stop_gained De novo - Simplex 27848944 Trujillano D , et al. (2016)
c.4012del p.Gly1338ValfsTer18 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.2318dupC p.Ser774ValfsTer12 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.4032delG p.Val1347TrpfsTer9 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.6533_6534insA p.Val2179fs frameshift_variant De novo - - 27620904 Martnez F , et al. (2016)
c.9682_9682delC p.Arg3228fs frameshift_variant De novo - - 27620904 Martnez F , et al. (2016)
c.6169del p.Val2057TyrfsTer18 frameshift_variant De novo - - 31044088 Chan AJS , et al. (2019)
c.1038delA p.Val347LeufsTer53 frameshift_variant De novo - - 25810209 Miyake N , et al. (2015)
c.2148delC p.Leu717CysfsTer39 frameshift_variant De novo - - 25810209 Miyake N , et al. (2015)
c.4599dup p.Lys1534Ter frameshift_variant De novo - Simplex 22795537 Jones WD , et al. (2012)
c.8267delT p.Leu2756Ter frameshift_variant De novo - Simplex 22795537 Jones WD , et al. (2012)
- - copy_number_loss De novo - Simplex 25533962 Deciphering Developmental Disorders Study (2014)
c.4667_4668del p.Cys1556SerfsTer2 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.6002_6005del p.Phe2001TrpfsTer8 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.74delG p.Gly26AlafsTer2 frameshift_variant De novo - Simplex 30841869 Zhang H , et al. (2019)
c.10324delG p.Ala3442ProfsTer17 frameshift_variant De novo - - 31044088 Chan AJS , et al. (2019)
c.3473G>A p.Cys1158Thr missense_variant De novo - Simplex 27848944 Trujillano D , et al. (2016)
c.3895_3896del p.Ser1299ProfsTer26 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.8174_8177del p.Glu2725ValfsTer22 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.9714_9735del p.Pro3239LeufsTer10 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.654_679delinsT p.Glu219LeufsTer27 frameshift_variant De novo - - 29574747 Baer S , et al. (2018)
c.11322-1G>A p.Lys3775SerfsTer32 splice_site_variant De novo - - 29203834 Lebrun N , et al. (2017)
c.7087_7090del p.Ser2363LeufsTer12 frameshift_variant De novo - - 31044088 Chan AJS , et al. (2019)
c.7695_7696del p.Glu2566LysfsTer14 frameshift_variant De novo - - 31044088 Chan AJS , et al. (2019)
c.3460C>T p.Arg1154Trp missense_variant Familial Paternal Multiplex 29574747 Baer S , et al. (2018)
c.6913delT p.Ser2305LeufsTer2 frameshift_variant De novo - Simplex 22795537 Jones WD , et al. (2012)
c.8806_8809delGTCT p.Val2936Ter frameshift_variant De novo - Simplex 22795537 Jones WD , et al. (2012)
c.8724del p.Glu2908AspfsTer21 frameshift_variant De novo - Simplex 30842647 Boonsawat P , et al. (2019)
c.9440C>T p.Ser3147Phe missense_variant Familial Maternal Multi-generational 29574747 Baer S , et al. (2018)
c.2758G>T p.Glu920Ter stop_gained De novo - Simplex 25533962 Deciphering Developmental Disorders Study (2014)
c.10850T>C p.Leu3617Pro missense_variant Familial Maternal Multi-generational 29574747 Baer S , et al. (2018)
c.6158delG;c.6167delG p.Arg2053fs;p.Arg2056fs frameshift_variant De novo - - 28263302 C Yuen RK , et al. (2017)
c.6571C>T p.Arg2191Ter stop_gained De novo - Simplex 25533962 Deciphering Developmental Disorders Study (2014)
c.7686_7687del;c.7695_7696del p.Ser2562fs;p.Ser2565fs frameshift_variant De novo - - 28263302 C Yuen RK , et al. (2017)
c.2124_2127delCTCTinsCT p.Ser709Ter frameshift_variant De novo - - 25533962 Deciphering Developmental Disorders Study (2014)
c.4205_4206insAGTGGACTTTAAGGTAAAGGTGTTCAGTGATCAT p.Arg1402fs frameshift_variant Unknown - - 28263302 C Yuen RK , et al. (2017)
c.10234dupT p.Tyr3412LeufsTer22 frameshift_variant De novo - Simplex 25533962 Deciphering Developmental Disorders Study (2014)
Common Variants  

No common variants reported.

SFARI Gene score
1S

High Confidence, Syndromic

1S

Score Delta: Score remained at 1.1 + S

1

High Confidence

See all Category 1 Genes

We considered a rigorous statistical comparison between cases and controls, yielding genome-wide statistical significance, with independent replication, to be the strongest possible evidence for a gene. These criteria were relaxed slightly for category 2.

The syndromic category includes mutations that are associated with a substantial degree of increased risk and consistently linked to additional characteristics not required for an ASD diagnosis. If there is independent evidence implicating a gene in idiopathic ASD, it will be listed as "#S" (e.g., 2S, 3S, etc.). If there is no such independent evidence, the gene will be listed simply as "S."

10/1/2017
1S
icon
1S

Score remained at 1S

Description

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in Jones et al., 2012 (PMID 22795537). Two additional de novo LoF variants in KMT2A were identified in ASD probands from the ASD: Genomes to Outcome Study cohort in Yuen et al., 2017 (PMID 28263302). Based on multiple de novo LoF variants in this gene, a probability of LoF intolerance rate (pLI) > 0.9, and higher-than-expected mutation rate (false discovery rate < 15%), KMT2A was determined to be an ASD candidate gene in Yuen et al., 2017. Mutations in this gene have also been identified in additional individuals presenting with developmental delay/intellectual disability (PMIDs 25533962, 27479843, 27848944)

4/1/2017
2S
icon
1S

Decreased from 2S to 1S

Description

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in PMID 22795537. Two additional de novo LoF variants in KMT2A were identified in ASD probands from the ASD: Genomes to Outcome Study cohort in Yuen et al., 2017. Based on multiple de novo LoF variants in this gene, a probability of LoF intolerance rate (pLI) > 0.9, and higher-than-expected mutation rate (false discovery rate < 15%), KMT2A was determined to be an ASD candidate gene in Yuen et al., 2017.

10/1/2016
2S
icon
2S

Decreased from 2S to 2S

Description

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in PMID 22795537.

7/1/2016
2S
icon
2S

Decreased from 2S to 2S

Description

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in PMID 22795537.

1/1/2016
2S
icon
2S

Decreased from 2S to 2S

Description

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in PMID 22795537.

1/1/2015
icon
2S

Increased from to 2S

Description

De novo loss-of-function variants in the KMT2A gene have been identified in ASD probands from three independent case cohorts: one from the Autism Sequencing Consortium (PMID 25363760), the second from the Simons Simplex Collection (PMID 25363768), and the third from the Deciphering Developmental Disorders Study (PMID 25533962). De novo mutations in this gene are also responsible for Wiedemann-Steiner syndrome (OMIM 605130), a disorder characterized by intellectual disability, excessive growth of terminal hair around the elbows (hypertrichosis cubiti), short stature, and a distinct facial appearance; autism was noted in 2/6 individuals with this syndrome in PMID 22795537.

Krishnan Probability Score

Score 0.61112172006711

Ranking 205/25841 scored genes


[Show Scoring Methodology]
Krishnan and colleagues generated probability scores genome-wide by using a machine learning approach on a human brain-specific gene network. The method was first presented in Nat Neurosci 19, 1454-1462 (2016), and scores for more than 25,000 RefSeq genes can be accessed in column G of supplementary table 3 (see: http://www.nature.com/neuro/journal/v19/n11/extref/nn.4353-S5.xlsx). A searchable browser, with the ability to view networks of associated ASD risk genes, can be found at asd.princeton.edu.
ExAC Score

Score 1

Ranking 9/18225 scored genes


[Show Scoring Methodology]
The Exome Aggregation Consortium (ExAC) is a summary database of 60,706 exomes that has been widely used to estimate 'constraint' on mutation for individual genes. It was introduced by Lek et al. Nature 536, 285-291 (2016), and the ExAC browser can be found at exac.broadinstitute.org. The pLI score was developed as measure of intolerance to loss-of- function mutation. A pLI > 0.9 is generally viewed as highly constrained, and thus any loss-of- function mutations in autism in such a gene would be more likely to confer risk. For a full list of pLI scores see: ftp://ftp.broadinstitute.org/pub/ExAC_release/release0.3.1/functional_gene_constraint/fordist_cle aned_exac_nonTCGA_z_pli_rec_null_data.txt
Iossifov Probability Score

Score 0.999

Ranking 4/239 scored genes


[Show Scoring Methodology]
Supplementary dataset S2 in the paper by Iossifov et al. (PNAS 112, E5600-E5607 (2015)) lists 239 genes with a probability of at least 0.8 of being associated with autism risk (column I). This probability metric combines the evidence from de novo likely-gene- disrupting and missense mutations and assesses it against the background mutation rate in unaffected individuals from the University of Washington’s Exome Variant Sequence database (evs.gs.washington.edu/EVS/). The list of probability scores can be found here: www.pnas.org/lookup/suppl/doi:10.1073/pnas.1516376112/- /DCSupplemental/pnas.1516376112.sd02.xlsx
Sanders TADA Score

Score 0.18886989801149

Ranking 105/18665 scored genes


[Show Scoring Methodology]
The TADA score ('Transmission and De novo Association') was introduced by He et al. PLoS Genet 9(8):e1003671 (2013), and is a statistic that integrates evidence from both de novo and transmitted mutations. It forms the basis for the claim of 65 individual genes being strongly associated with autism risk at a false discovery rate of 0.1 (Sanders et al. Neuron 87, 1215-1233 (2015)). The calculated TADA score for 18,665 RefSeq genes can be found in column P of Supplementary Table 6 in the Sanders et al. paper (the column headed 'tadaFdrAscSscExomeSscAgpSmallDel'), which represents a combined analysis of exome data and small de novo deletions (see www.cell.com/cms/attachment/2038545319/2052606711/mmc7.xlsx).
CNVs associated with KMT2A(1 CNVs)
11q23.3 14 Deletion-Duplication 26  /  40
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