About ATM
No gene-level summary was recorded for this case.
Previous versions
Variant interpretation report
ATM c.2873A>G, p.(Glu958Gly)
Classification
Benign
Variant description:
No variant summary was recorded for this case.
Five-step scale from benign to pathogenic. This variant is benign. Select a step to read what it means.
Benign.A benign classification under the recorded framework.
In plain language
Gene-level background from the recorded interpretation.
Words with a dotted underline have a short definition. Hover or tap them.
LYFE Sciences is an AI system, and it can make mistakes.
Criteria may be applied incorrectly, sources may be misread, and a
confident-looking classification can still be wrong.
Double-check every criterion and its underlying evidence
before relying on any call.
01The reasoning
How it was classified
The recorded framework is ClinGen ATM VCEP v1.5.0. The criteria and strengths shown below come from the saved assessment; this page does not recalculate the classification.
Recorded applied criteria
The applied criteria and their strengths are shown as assessed under the stated framework.
Pathogenic evidence criteria: 0
Benign evidence criteria: 4
Pathogenic criteria applied · 0
No pathogenic criterion marked as applied in the recorded assessment.
Benign criteria applied · 4
BS1Strong
BS1 · strong
gnomAD v4.1 grpmax filtering allele frequency is 0.0752% (FAF=0.000752), exceeding the VCEP BS1 threshold of >0.05%. The variant is present on 90 alleles including one homozygous individual, indicating it is more common than expected for a highly penetrant ATM pathogenic variant.
BS3Moderate
BS3 · moderate
Comprehensive functional assessment of all ATM SNVs using prime editing and deep learning (PMID:40580951) classifies c.2873A>G (p.Glu958Gly) as 'Functional' with high confidence (combined score -0.866). The variant rescues both ATM-specific phosphorylation activity and radiosensitivity, meeting VCEP BS3_Moderate criteria. Prior independent studies (Barone et al. 2009, Mitui et al. 2009) also reported normal kinase activity and radiosensitivity for this variant.
BP2Strong
BP2 · strong
c.2873A>G has been observed in cis with a known pathogenic ATM variant (c.5932G>T, p.Glu1978*) on the same allele. Under the ATM VCEP PM3/BP2 table, confirmed cis configuration with a pathogenic variant in a recessive gene assigns -4.0 points, corresponding to BP2_Strong.
BP4Supporting
BP4 · supporting
REVEL score is 0.121, below the VCEP BP4 missense threshold of ≤0.249. BayesDel score is -0.224, consistent with a benign computational prediction. SpliceAI predicts no significant splice impact (max delta 0.19).
Recorded classification: Benign
Richards et.al., 2015 - Combining rules v1.5.0 criteria-combination framework: matched Rule16 (Benign.Strong >=2) with applied criteria: BS1 strong, BS3 moderate, BP2 strong, BP4 supporting; maps to Benign.
02The sources
Evidence at a glance
Evidence summaries and captured source records, where available. Missing entries should not be interpreted as negative findings.
gnomAD v4.1
gnomAD v2.1
Population frequency
90 / 1,614,012 alleles
gnomAD v4.1: 90 / 1,614,012 alleles. Recorded AF 5.57617e-05. Recorded homozygote count 1.
gnomAD v2.1
This variant is present in gnomAD v2.1 (AF= 9.5457e-05; MAF= 0.00955%, 24/251422 alleles, homozygotes = 0) and has highest observed frequency in the South Asian population (AF= 0.000718672; MAF= 0.07187%, 22/30612 alleles, homozygotes = 0); grpmax FAF= 0.00048585.
SpliceAI score
0.190 maximum delta
Recorded SpliceAI maximum delta score: 0.190. Refer to the recorded PP3/BP4 rationale for interpretation.
ClinVar submissions
9 reported laboratory submissions
6 Uncertain significance · 3 Likely benign.
Context only
ClinVar ↗
Functional evidence
Statement recorded
OncoKB did not identify variant-specific reviewed functional evidence for this variant; gene-level curated context is available for reviewer follow-up. ATM, a kinase involved in the DNA damage response, is mutated in various solid and hematologic malignancies.
COSMIC
Cancer Hotspots
Somatic evidence
No matching record reported
This variant has not previously been reported in somatic cancers (COSMIC).
Cancer Hotspots
This variant does not lie in a statistically significant hotspot.
Context only
For specialists
Technical detail
ACMG/AMP criteria under ClinGen ATM VCEP v1.5.0, with the data and sources behind each one.
29 criteria with recorded statuses: 4 met · 7 not met · 0 not assessed · 18 not applicable. Open any row for the full reasoning, the rule and the evidence behind it.
Met
Not met
Not assessed
Not applicable
BS1_Strong: The variant is present in gnomAD v4.1 at a grpmax filtering allele frequency of 0.0752%, exceeding the ATM VCEP threshold of >0.05% for BS1. The variant has been observed on 90 alleles including one homozygous individual, with highest frequency in the South Asian population (0.091%).
BS3_Moderate: Comprehensive functional assessment of all ATM SNVs using prime editing and deep learning (PMID:40580951) classifies p.Glu958Gly as 'Functional' with high confidence. The variant rescues both ATM-specific phosphorylation activity and radiosensitivity, meeting VCEP criteria for BS3_Moderate.
BP2_Strong: c.2873A>G has been observed in cis with a known pathogenic ATM variant (c.5932G>T, p.Glu1978*) on the same allele, corresponding to -4.0 points (BP2_Strong) under the ATM VCEP PM3/BP2 table.
BP4_Supporting: REVEL score of 0.121 is below the VCEP benign threshold of ≤0.249. BayesDel score of -0.224 is consistent with a benign prediction. SpliceAI predicts no significant splice impact (max delta 0.19).
No pathogenic criteria were met: PVS1 is not applicable (missense variant). PS1 is not met (no same amino acid change classified as pathogenic at codon 958). PS3 is not met (functional studies show normal, not damaging, effect). PM2 is not met (AF=0.00558% exceeds ≤0.001% VCEP threshold). PP3 is not met (REVEL=0.121 below >0.7333 threshold; SpliceAI=0.19 below ≥0.2 threshold).
No criteria match.
Met · 4
BS1 StronggnomAD v4.1 grpmax filtering allele frequency is 0.0752% (FAF=0.000752), exceeding the VCEP BS1 threshold of >0.05%. The variant is present on 90 alleles including one homozygous individual, indicating it is more common than expected for a highly penetrant ATM pathogenic variant. Details ▾Hide ▴
Evidence considered
- gnomAD v4.1: grpmax FAF=0.000752 (0.0752%)
- exceeding VCEP BS1 threshold of >0.05%. 90 alleles
- 1 homozygote. Highest in South Asian population (AF=0.0911%).
Sources
BS3 ModerateComprehensive functional assessment of all ATM SNVs using prime editing and deep learning (PMID:40580951) classifies c.2873A>G (p.Glu958Gly) as 'Functional' with high confidence (combined score -0.866). The variant rescues both ATM-specific phosphorylation activity and radiosensitivity, meeting VCEP BS3_Moderate criteria. Prior independent studies (Barone et al. 2009, Mitui et al. 2009) also reported normal kinase activity and radiosensitivity for this variant. Details ▾Hide ▴
Evidence considered
- PMID:40580951 Suppl Table S1: E958G classified as 'Functional'
- High confidence
- combined score -0.866. Rescues both ATM-specific phosphorylation and radiosensitivity. Prior studies corroborate normal function.
Sources
BP2 Strongc.2873A>G has been observed in cis with a known pathogenic ATM variant (c.5932G>T, p.Glu1978*) on the same allele. Under the ATM VCEP PM3/BP2 table, confirmed cis configuration with a pathogenic variant in a recessive gene assigns -4.0 points, corresponding to BP2_Strong. Details ▾Hide ▴
Evidence considered
- Observed in cis with pathogenic ATM variant c.5932G>T (p.Glu1978*). VCEP BP2 table: confirmed in cis = -4.0 points = BP2_Strong.
Still missing
- Cis observation not independently verified in published literature
- derived from ClinVar submitter evidence as noted in ATM VCEP curation.
Sources
vcep_atm_pm3_bp2_1_5
BP4 SupportingREVEL score is 0.121, below the VCEP BP4 missense threshold of ≤0.249. BayesDel score is -0.224, consistent with a benign computational prediction. SpliceAI predicts no significant splice impact (max delta 0.19). Details ▾Hide ▴
Evidence considered
- REVEL=0.121 (≤0.249 VCEP BP4 threshold). BayesDel=-0.224 (benign). SpliceAI max_delta=0.19 (no significant splice impact).
Sources
Not met · 7 · evaluated, threshold not reached
PS1 No known pathogenic or likely pathogenic variant with the same amino acid change (p.Glu958Gly) has been identified. Other nucleotide substitutions at codon 958 produce different amino acid changes (p.Glu958Val, p.Glu958Ala), which are not the same amino acid substitution required for PS1. Details ▾Hide ▴
Evidence considered
- ATM codon 958: only c.2873A>T (E958V) and c.2873A>C (E958A) observed as alternate nucleotide changes
- neither encodes the same amino acid change (E958G) and neither is classified as pathogenic.
Sources
vcep_atm_ps1_1_5vcep_suppl_tables1_pmid_4058095140580951
PS3 Well-established functional studies demonstrate normal ATM kinase activity and normal radiosensitivity for p.Glu958Gly, supporting a benign functional effect rather than a damaging one. The variant is classified as 'Functional' with high confidence in the ATM VCEP functional assessment dataset (PMID:40580951). Details ▾Hide ▴
Evidence considered
- PMID:40580951 Suppl Table S1 classifies c.2873A>G (E958G) as 'Functional' with combined score -0.866 and 'High' confidence
- indicating normal protein function. Exploratory evidence notes Barone et al. 2020 and Mitui et al. 2009 also reported normal kinase activity and radiosensitivity.
Sources
PS4 No case-control study or large case series demonstrating statistically significant enrichment of c.2873A>G in affected individuals compared to controls has been identified. The VCEP PS4 rule requires p≤0.05 AND (OR≥2 OR lower 95% CI ≥1.5). Details ▾Hide ▴
Evidence considered
- Variant is rare (gnomAD v4.1 AF=0.00558%) with no case-control studies demonstrating significant odds ratio.
Still missing
- No case-control study or enriched case series available for this variant.
Sources
PM2 gnomAD v4.1 allele frequency is 5.58×10⁻⁵ (0.00558%, 90/1,614,012 alleles), which exceeds the VCEP PM2_Supporting threshold of ≤0.001% (≤1×10⁻⁵). Details ▾Hide ▴
Evidence considered
- gnomAD v4.1: AF=5.58×10⁻⁵ (0.00558%)
- 90 alleles
- 1 homozygote. Exceeds VCEP PM2 threshold of ≤0.001%.
Sources
PP1 No published co-segregation data for c.2873A>G in families with multiple affected members has been identified. No LOD score is available. Details ▾Hide ▴
Evidence considered
- No co-segregation data found for this variant.
Still missing
- No co-segregation or family studies available.
PP3 REVEL score is 0.121, well below the VCEP PP3 threshold of >0.7333 for missense variants. SpliceAI max delta score is 0.19, below the splicing threshold of ≥0.2. Details ▾Hide ▴
Evidence considered
- REVEL=0.121 (<0.7333 threshold). SpliceAI max_delta=0.19 (<0.2 threshold). BayesDel=-0.224 (benign prediction).
Sources
revelspliceai ↗
BA1 gnomAD v4.1 grpmax filtering allele frequency is 0.0752% (FAF=0.000752), which does not exceed the VCEP BA1 threshold of >0.5%. Details ▾Hide ▴
Evidence considered
- gnomAD v4.1 grpmax FAF=0.000752 (0.0752%)
- below BA1 threshold of >0.5%.
Sources
Not applicable · 18· recorded as not applicable Show reasons ▾Hide reasons ▴
PVS1 N/AMissense variant (p.Glu958Gly); PVS1 is reserved for null variants (nonsense, frameshift, canonical splice, initiation codon, exon deletion) per the ATM PVS1 Decision Tree. A missense substitution does not qualify. Details ▾Hide ▴
Evidence considered
- Variant is a missense substitution (c.2873A>G
- p.E958G)
- not a null variant eligible for PVS1.
Sources
pvs1_variant_assessmentvcep_atm_pvs1_1_5
PS2 VCEPVCEP states do not use for AD or AR disease; informative de novo occurrences have not yet been observed and de novo AR conditions are unlikely to be informed by phase. Details ▾Hide ▴
No further detail was recorded.
PM1 VCEPVCEP states do not use: benign and pathogenic variants are known to occur within the same ATM domains and germline mutational hotspots are not well defined at this time. Details ▾Hide ▴
No further detail was recorded.
PM3 N/ASkipped per case adjudication directive; PM3 trans observation data was not assessed as part of this criteria review. Details ▾Hide ▴
No further detail was recorded.
PM4 N/AVCEP PM4 rule applies to stop-loss variants only. This is a missense substitution (c.2873A>G, p.Glu958Gly), not a stop-loss variant. Details ▾Hide ▴
No further detail was recorded.
PM5 N/AVCEP PM5 rule applies only to frameshifting or truncating variants with premature termination codons upstream of p.Arg3047, or splice variants with PVS1_Strength(RNA). Missense changes are explicitly excluded: 'Do not use for missense changes.' Details ▾Hide ▴
Evidence considered
- Variant is a missense substitution (p.E958G)
- PM5 restricted to truncating/splice variants per VCEP.
Sources
pm5_candidates
PM6 VCEPVCEP states do not use for AD or AR disease: informative de novo occurrences have not yet been observed and de novo AR conditions are unlikely to be informed by phase. Details ▾Hide ▴
No further detail was recorded.
PP2 VCEPVCEP states do not use: ATM does not have a defined low rate of missense benign variation. Details ▾Hide ▴
No further detail was recorded.
PP4 VCEPVCEP states do not use: AD condition has multiple genetic etiologies; AR condition phenotype evidence is built into the PM3/BP2 table. Details ▾Hide ▴
No further detail was recorded.
PP5 VCEPVCEP states this criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee. Details ▾Hide ▴
No further detail was recorded.
BS2 VCEPVCEP states do not use: ATM has incomplete penetrance. Details ▾Hide ▴
No further detail was recorded.
BS4 VCEPVCEP states do not use: co-segregation analysis in low-penetrance genes can lead to false positive results (AD); informative instances of lack of co-segregation in A-T families are too rare (AR). Details ▾Hide ▴
No further detail was recorded.
BP1 VCEPVCEP states do not use: missense pathogenic variants are known for ATM. Details ▾Hide ▴
No further detail was recorded.
BP3 VCEPVCEP states do not use. BP3 applies to in-frame deletions/insertions in repetitive regions without known function; this is a single-nucleotide missense substitution. Details ▾Hide ▴
No further detail was recorded.
BP5 VCEPVCEP states do not use: cases with multiple pathogenic variants have been observed with no noticeable difference in phenotype; ATM has low penetrance and will naturally occur with other pathogenic variants more frequently. Details ▾Hide ▴
No further detail was recorded.
BP6 VCEPVCEP states this criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee. Details ▾Hide ▴
No further detail was recorded.
BP7 N/ABP7 applies to synonymous and deep intronic variants only. This is a missense variant (c.2873A>G, p.Glu958Gly) resulting in an amino acid substitution, not a silent substitution. Details ▾Hide ▴
Evidence considered
- Variant is missense (p.E958G)
- not synonymous or deep intronic.
PS5 N/APS5 is not a standard ACMG/AMP criterion and is not defined in the ATM VCEP v1.5.0 framework. Details ▾Hide ▴
No further detail was recorded.
Identifiers
- Gene
- ATM
- Transcript
- NM_000051.4
- Coding (HGVS c.)
- NM_000051.4:c.2873A>G
- Protein (HGVS p.)
- NP_000042.3:p.(Glu958Gly)
- GRCh38
- chr11:108271098 A>G
- GRCh37
- chr11:108141825 A>G
- ClinVar
- 133611
Gene diagram
Every interpreted variant in ATM, mapped onto the exon structure of NM_000051.4. Select a row to find it on the plot.
ATMNM_000051.4
Fetching transcript structure from UCSC…
Exons
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Transcript span
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Strand
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Variants mapped
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Source
UCSC ncbiRefSeqCurated
All variants in ATM
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Select a row to find it on the plot; use the link to open its page.
| Protein | Location | Classification | Link |
|---|
gnomAD v4.1
90 / 1,614,012 alleles
AF 5.58e-05 · 1 homozygotes · FAF 0.000752
gnomAD v2.1
24 / 251,422 alleles
AF 9.55e-05 · 0 homozygotes · FAF 0.000486
gnomAD-Canada v1.0
0 / 0 alleles
AF 0 · 0 homozygotes · FAF 0
By genetic ancestry
gnomAD v4.1
AF 5.6e-05 · 90 / 1,614,012 alleles · 1 hom · FAF 0.00075
| South Asian83 / 91,088 | 0.000911 hom |
| Remaining individuals3 / 62,488 | 4.8e-05 |
| Admixed American1 / 59,996 | 1.7e-05 |
| African/African American1 / 74,918 | 1.3e-05 |
| European (non-Finnish)2 / 1,180,036 | 1.7e-06 |
0 alternate alleles recorded in 5 other groups: European (Finnish), Amish, East Asian, Middle Eastern, Ashkenazi Jewish.
gnomAD v2.1
AF 9.5e-05 · 24 / 251,422 alleles · 0 hom · FAF 0.00049
| South Asian22 / 30,612 | 0.00072 |
| Admixed American1 / 34,590 | 2.9e-05 |
| European (non-Finnish)1 / 113,732 | 8.8e-06 |
0 alternate alleles recorded in 5 other groups: African/African American, Ashkenazi Jewish, East Asian, European (Finnish), Remaining individuals.
gnomAD-Canada
AF 0 · 0 / 0 alleles · 0 hom
Statements
gnomAD v4.1
This variant is present in gnomAD v4.1 (AF= 5.57617e-05; MAF= 0.00558%, 90/1614012 alleles, homozygotes = 1) and has highest observed frequency in the South Asian population (AF= 0.000911207; MAF= 0.09112%, 83/91088 alleles, homozygotes = 1); grpmax FAF= 0.00075231.
gnomAD v2.1
This variant is present in gnomAD v2.1 (AF= 9.5457e-05; MAF= 0.00955%, 24/251422 alleles, homozygotes = 0) and has highest observed frequency in the South Asian population (AF= 0.000718672; MAF= 0.07187%, 22/30612 alleles, homozygotes = 0); grpmax FAF= 0.00048585.
SpliceAI and Pangolin
Other predictors
- REVEL
- 0.121
- BayesDel
- -0.224
How the predictions were used
BP4 SupportingREVEL score is 0.121, below the VCEP BP4 missense threshold of ≤0.249. BayesDel score is -0.224, consistent with a benign computational prediction. SpliceAI predicts no significant splice impact (max delta 0.19). Details ▾Hide ▴
Evidence considered
- REVEL=0.121 (≤0.249 VCEP BP4 threshold). BayesDel=-0.224 (benign). SpliceAI max_delta=0.19 (no significant splice impact).
Sources
PP3 REVEL score is 0.121, well below the VCEP PP3 threshold of >0.7333 for missense variants. SpliceAI max delta score is 0.19, below the splicing threshold of ≥0.2. Details ▾Hide ▴
Evidence considered
- REVEL=0.121 (<0.7333 threshold). SpliceAI max_delta=0.19 (<0.2 threshold). BayesDel=-0.224 (benign prediction).
Sources
revelspliceai ↗
BP7 N/ABP7 applies to synonymous and deep intronic variants only. This is a missense variant (c.2873A>G, p.Glu958Gly) resulting in an amino acid substitution, not a silent substitution. Details ▾Hide ▴
Evidence considered
- Variant is missense (p.E958G)
- not synonymous or deep intronic.
Statement
In silico
SpliceAI predicts no significant splice impact for this variant (max delta score = 0.19). REVEL score = 0.121. BayesDel score = -0.224243.
10 paper records listed. No publication is explicitly linked to an applied criterion in the recorded metadata. None of the listed paper records explicitly indicates that the variant is named.
Recorded publications
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PMID 25741868 ↗Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology.No paper-specific finding is recorded.
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PMID 40580951 ↗Functional assessment of all ATM SNVs using prime editing and deep learning.Lee KS et al. · 2025No paper-specific finding is recorded.
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PMID 20301317 ↗Hereditary Ataxia Overview.Adam MP et al. · 1993No paper-specific finding is recorded.
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PMID 20301790 ↗Ataxia-Telangiectasia.Adam MP et al. · 1993No paper-specific finding is recorded.
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PMID 24418350 ↗EFNS/ENS Consensus on the diagnosis and management of chronic ataxias in adulthood.No paper-specific finding is recorded.
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PMID 24728327 ↗Germline variation in cancer-susceptibility genes in a healthy, ancestrally diverse cohort: implications for individual genome sequencing.No paper-specific finding is recorded.
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PMID 25394175 ↗A practice guideline from the American College of Medical Genetics and Genomics and the National Society of Genetic Counselors: referral indications for cancer predisposition assessment.Hampel H et al. · 2015No paper-specific finding is recorded.
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PMID 26389210 ↗Genetics of Breast and Gynecologic Cancers (PDQ®): Health Professional Version.PDQ Cancer Genetics Editorial Board · 2002No paper-specific finding is recorded.
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PMID 20050888 ↗EFNS guidelines on the molecular diagnosis of ataxias and spastic paraplegias.Gasser T et al. · 2010No paper-specific finding is recorded.
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PMID 28492532 ↗Sherloc: a comprehensive refinement of the ACMG-AMP variant classification criteria.No paper-specific finding is recorded.
Screenshots represent source records captured during evidence collection. Select one to view the recorded source content.
gnomAD v4.1
90 / 1,614,012 recorded alleles
Open source ↗
gnomAD v2.1
Captured gnomAD v2.1 source record
Open source ↗
SpliceAI Lookup
Recorded maximum delta 0.190
Open source ↗
ClinVar
6 Uncertain significance · 3 Likely benign
Open source ↗
COSMIC
Captured COSMIC source record
Open source ↗
Cancer hotspots
Captured Cancer Hotspots source record
Open source ↗
OncoKB
Captured OncoKB source record
Open source ↗
ClinGen CSpec
Captured ClinGen CSpec source record
Open source ↗
All source links
- ClinGen CSpec ↗cspec.genome.network/cspec/ui/svi/doc/639508985
- ClinVar ↗www.ncbi.nlm.nih.gov/clinvar/variation/133611/
- gnomAD v2.1 ↗gnomad.broadinstitute.org/variant/11-108141825-A-G?dataset=gnom…
- gnomAD v4.1 ↗gnomad.broadinstitute.org/variant/chr11-108271098-A-G?dataset=g…
- SpliceAI Lookup ↗spliceailookup.broadinstitute.org/#variant=NM_000051.4%3Ac.2873…
- OncoKB ↗www.oncokb.org/gene/ATM/E958G
- COSMIC ↗cancer.sanger.ac.uk/cosmic/search?q=ATM+c.2873A%3EG
- Cancer hotspots ↗www.cancerhotspots.org/
Statements for reports
The evidence statements recorded by the interpretation pipeline. They have not been reinterpreted by the page.
gnomAD v4.1
This variant is present in gnomAD v4.1 (AF= 5.57617e-05; MAF= 0.00558%, 90/1614012 alleles, homozygotes = 1) and has highest observed frequency in the South Asian population (AF= 0.000911207; MAF= 0.09112%, 83/91088 alleles, homozygotes = 1); grpmax FAF= 0.00075231.
gnomAD v2.1
This variant is present in gnomAD v2.1 (AF= 9.5457e-05; MAF= 0.00955%, 24/251422 alleles, homozygotes = 0) and has highest observed frequency in the South Asian population (AF= 0.000718672; MAF= 0.07187%, 22/30612 alleles, homozygotes = 0); grpmax FAF= 0.00048585.
ClinVar
This variant has been reported in ClinVar as Uncertain significance (6 clinical laboratories) and as Likely benign (3 clinical laboratories). (ClinVarID = 133611)
In silico
SpliceAI predicts no significant splice impact for this variant (max delta score = 0.19). REVEL score = 0.121. BayesDel score = -0.224243.
Functional
OncoKB did not identify variant-specific reviewed functional evidence for this variant; gene-level curated context is available for reviewer follow-up. ATM, a kinase involved in the DNA damage response, is mutated in various solid and hematologic malignancies.
Somatic
This variant does not lie in a statistically significant hotspot. This variant has not previously been reported in somatic cancers (COSMIC).
Cancer Hotspots
This variant does not lie in a statistically significant hotspot.