ReviewNature genetics2026
The inactive X chromosome as a female protector in autism and beyond.
Review in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Immune markers mediate genetic relationships between immune diseases and psychiatric disorders.PLoS genetics · 2026Article
- Neurodevelopmental outcomes relevant to autism in juvenile mice exposed to PCB 11 in the maternal diet throughout gestation and lactation.Frontiers in toxicology · 2026Article
Corrections and comments
- Update of
Authors and funding
2 authors.
Funding
Abstract
Female individuals require greater autosomal genetic risk than male individuals to manifest autism, yet the biological basis of this 'female protective effect' (FPE) remains unknown. Based on insights into the human sex chromosomes, we propose that the FPE arises from higher expression of a subset of X-linked genes in females due to transcription from both the active (Xa) and inactive (Xi) X chromosomes. These higher expression levels enable females to buffer mutations in autosomal genes and in pathways regulated by Xi-expressed genes. This framework unifies epidemiological, genetic and mechanistic observations across autism and other male-biased congenital and developmental disorders, suggesting that the combined activity of Xa and Xi allows females to better tolerate autosomal genetic risk across many pediatric conditions. If correct, this reshapes our understanding of sex differences in human disease and positions Xi as a genetic suppressor of autosomal mutations in autism and beyond.
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Registered trials
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 OpenQuestion graph.