NF1 encodes neurofibromin, a tumor suppressor protein that negatively regulates the RAS signal transduction pathway. As a GTPase-activating protein, it helps switch RAS proteins from their active to inactive state, keeping cell growth in check; loss of NF1 function leaves RAS overactive and drives downstream growth pathways such as MAPK/ERK and PI3K. Inherited changes in NF1 cause the cancer-predisposition syndrome neurofibromatosis type 1, and are also linked to juvenile myelomonocytic leukemia and Watson syndrome. Somatic changes in NF1 are found in many tumor types, including breast cancer, melanoma, and glioma.
This variant
NF1 encodes neurofibromin, a RAS-pathway tumor suppressor, and inherited NF1 variants cause neurofibromatosis type 1 through loss of growth control.
Transcript
NM_001042492.2
HGVS · transcript:coding
NM_001042492.2:c.7584A>G
GRCh38
chr17:31352383 A>G
GRCh37
chr17:29679401 A>G
Likely Benign: BS2 (strong), BP4 (supporting), and BP7 (supporting) satisfy the generic ACMG/AMP fallback combination of one strong plus one supporting benign criterion.
Classification rationale
BS2BP4BP7Likely Benign
NF1 c.7584A>Gsynonymous · exon 51
BS2 strong: gnomAD v4.1 reports six homozygotes, inconsistent with a highly penetrant autosomal-dominant NF1 allele. BP4 supporting: SpliceAI maximum delta 0.001 predicts no splice impact. BP7 supporting: the synonymous variant is outside the canonical splice consensus with minimal predicted splice impact.
BS2 + BP4 + BP7→Likely Benign
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.
Gene diagram
· NM_001042492.2 · variants mapped to exon structure
NF1NM_001042492.2
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 NF1—click a row to locate it on the plot · use the link column to open its page
Protein
Location
Classification
Link
Applied criteria · 3 applied · 16 assessed
MetEvidence satisfies this criterion.
Not metEvaluated against available evidence; threshold not reached.
Not assessedApplies in principle, but no evidence was found to evaluate it.
N/ADoesn't apply to this variant type.
Applied · 3
Strength Supporting Moderate Strong Very strong
✓
BS2strongreviewBenign
Met: gnomAD v4.1 contains 6 homozygotes, incompatible with a highly penetrant autosomal-dominant NF1 allele.
The governing NF1 framework identifies autosomal-dominant inheritance for neurofibromatosis type 1.gnomAD v4.1 reports total_hom 6, comprising 5 exome homozygotes and 1 genome homozygote, among 1578/1614034 observed alleles.The absence of individual-level phenotype and age data prevents direct confirmation of the ACMG/AMP healthy-adult wording and is the reason for human review.
Met, supporting: synonymous variant has a SpliceAI maximum delta score of 0.001, meeting the <=0.1 BP4 threshold.
The case variant is NM_001042492.2:c.7584A>G, annotated as synonymous, NP_001035957.1:p.(Gln2528=).SpliceAI is available and reports maximum delta 0.001.The supplied Jaganathan et al. 2019 calibration (PMID:30661751) defines BP4 supporting for SpliceAI max delta <=0.1.
Met, supporting: synonymous c.7584A>G is non-canonical and has a minimal SpliceAI maximum delta score of 0.001.
The variant is synonymous, NM_001042492.2:c.7584A>G, p.(Gln2528=).The case assessment identifies the variant as outside the canonical splice consensus, and SpliceAI reports maximum delta 0.001.The ACMG/AMP guideline basis for BP7 is Richards et al. 2015 (PMID:25741868): a synonymous variant may support benign evidence when it is not expected to affect splicing.
This variant is present in gnomAD v4.1 (AF= 0.000977675; MAF= 0.09777%, 1578/1614034 alleles, homozygotes = 6) and has highest observed frequency in the Middle Eastern population (AF= 0.00792602; MAF= 0.79260%, 48/6056 alleles, homozygotes = 0); grpmax FAF= 0.0061424.
v2.1
This variant is present in gnomAD v2.1 (AF= 0.00109648; MAF= 0.10965%, 310/282724 alleles, homozygotes = 0) and has highest observed frequency in the Ashkenazi Jewish population (AF= 0.00694578; MAF= 0.69458%, 72/10366 alleles, homozygotes = 0); grpmax FAF= 0.00159181.
This variant has been reported in ClinVar as Likely benign (12 clinical laboratories) and as Benign (7 clinical laboratories) and as Uncertain significance (1 clinical laboratory). (ClinVarID = 184154)
This variant does not lie in a statistically significant hotspot. This variant has previously been reported in somatic cancers (COSMIC; COSV62204673, n = 1 times).
Hotspots
This variant does not lie in a statistically significant hotspot.
Each card is an audit: what was searched, what was found, whether it names the variant, which criteria it fed, and why. 9 further PMIDs triaged but not cited — see Sources & references.
Rule & framework references · cited for criterion definitions, not variant evidence
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.
Sources & reference links
9Sources
CSpec VCEP
ClinVar
gnomAD v2.1
gnomAD v4.1
gnomAD-Canada
SpliceAI
OncoKB
COSMIC
Cancer hotspots
Triaged references · 9 PMIDs not cited in assessment
23460398 ↗Neurofibromatosis-1 gene deletions and mutations in de novo adult acute myeloid leukemia.CLINVAR
24033266 ↗A systematic approach to assessing the clinical significance of genetic variants.CLINVAR
10678181 ↗Nf1 and Gmcsf interact in myeloid leukemogenesis.CLINVAR
20065170 ↗American Society of Clinical Oncology policy statement update: genetic and genomic testing for cancer susceptibility.CLINVAR
26324357 ↗American Society of Clinical Oncology Policy Statement Update: Genetic and Genomic Testing for Cancer Susceptibility.CLINVAR
26140447 ↗Points to Consider: Ethical, Legal, and Psychosocial Implications of Genetic Testing in Children and Adolescents.CLINVAR
28492532 ↗Sherloc: a comprehensive refinement of the ACMG-AMP variant classification criteria.CLINVAR
33939658 ↗The North American Neuroendocrine Tumor Society Consensus Guidelines for Surveillance and Management of Metastatic and/or Unresectable Pheochromocytoma and Paraganglioma.CLINVAR