Evidence map›Paper›PMID 41786677›Full record

ArticleClinical genetics2026

Functional Data Strengthen Clinical Validation of PhenoScore Phenotype-Guided AI for ANKRD11 Missense Variants.

Evi Andriessen, Elke de Boer, Gholson J Lyon, Bert B A de Vries, Charlotte W Ockeloen, Alexander J M Dingemans

Abstract read
In one paragraph

Article in Clinical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Evi AndriessenDepartment of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.
Elke de BoerDepartment of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.
Gholson J LyonNew York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.ORCID 0000-0002-5869-0716
Bert B A de VriesDepartment of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.
Charlotte W OckeloenDepartment of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.ORCID 0000-0003-0329-1520
Alexander J M DingemansDepartment of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.ORCID 0000-0002-5648-2155

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KBG syndrome (KBGS, OMIM #148050) is a rare genetic disorder caused by heterozygous truncating or missense variants in the ANKRD11 gene or a deletion of 16q24.3 involving ANKRD11. While truncating variants clearly disrupt protein function, the interpretation of missense variants is more challenging, as many remain variants of uncertain significance (VUS). To address this, we evaluated PhenoScore, an open-source AI-based phenomics framework integrating facial recognition and medical data analysis, for predicting the pathogenicity of ANKRD11 missense variants and providing supporting evidence for variant interpretation within the ACMG framework, specifically the PP4 criterion. PhenoScore was trained on 79 individuals with truncating variants in ANKRD11 and age-, sex-, and ethnicity-matched controls with other neurodevelopmental disorders, and its performance was compared to AlphaMissense, REVEL, and the evaluation of a clinical geneticist. Six individuals with functionally confirmed pathogenic missense variants were used for testing. PhenoScore achieved high predictive accuracy with an area under the curve (AUC) of 0.95 and a Brier score of 0.089, and pathogenic missense variants in the test set received a mean prediction score of 0.94. PhenoScore significantly outperformed REVEL (p < 0.01), especially in cases supported by functional and clinical evidence, while no significant difference was observed compared to AlphaMissense (p = 0.63); importantly, the two tools showed complementary strengths. These findings suggest that PhenoScore represents a promising tool for clinical variant interpretation, as it quantifies phenotypic concordance with KBGS and provides objective evidence that can strengthen the PP4 criterion within the ACMG framework. Combined with molecular prediction tools like AlphaMissense, PhenoScore may help reduce uncertainty surrounding VUS in ANKRD11 by complementing these scores.

Indexed as

Abnormalities, MultipleArtificial IntelligenceCraniofacial AbnormalitiesIntellectual DisabilityMutation, MissenseRepressor ProteinsAdolescentBone Diseases, DevelopmentalChildFaciesFemaleGenetic Association StudiesHumansMalePhenotypeTooth AbnormalitiesANKRD11 protein, humanRepressor Proteinsartificial intelligenceKBG syndromenext‐generation phenotypingPhenoScore

Identifiers

PMID41786677
PMCPMC13167626

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.