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Understanding how disruptions to these functionally diverse genes lead to the core features of ASD remains a major challenge\n                    <jats:sup>4<\/jats:sup>\n                    . Moreover, ASD is three- to four-fold more common in male than in female individuals\n                    <jats:sup>5<\/jats:sup>\n                    , and female autistic people tend to carry more autosomal risk alleles for ASD compared with their male counterparts\n                    <jats:sup>6,7<\/jats:sup>\n                    ; however, the biological basis of this \u2018female protective effect\u2019 (FPE) has remained unknown\n                    <jats:sup>8,9<\/jats:sup>\n                    . Here we show that individual perturbations of 18 ASD genes in human neural progenitor cells converge on shared effects on gene expression, including widespread downregulation of other ASD genes. De novo reconstruction of a gene regulatory network enabled identification of central transcriptional regulators that drive this transcriptomic convergence, including prominent ASD gene\n                    <jats:italic>CHD8<\/jats:italic>\n                    and candidates including\n                    <jats:italic>REST<\/jats:italic>\n                    . Furthermore, X-linked transcription factor ZFX, which is expressed from both the active and the\u00a0inactive X chromosomes in female individuals\n                    <jats:sup>10<\/jats:sup>\n                    , emerged as a key activator of many ASD genes: we propose that the higher\n                    <jats:italic>ZFX<\/jats:italic>\n                    expression level observed in the female brain can buffer damaging mutations in diverse ASD genes, contributing to the female protective effect. Together, these results show how key gene regulatory networks can become broadly and similarly dysregulated upon disruption of individual ASD genes and provide molecular insight into the female protective effect in ASD.\n                  <\/jats:p>","DOI":"10.1038\/s41586-026-11236-6","type":"journal-article","created":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T16:02:53Z","timestamp":1793808173000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Transcriptomic convergence and the female protective effect in autism"],"prefix":"10.1038","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0702-3120","authenticated-orcid":false,"given":"Rebecca E.","family":"Andersen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maya","family":"Talukdar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-5972-8288","authenticated-orcid":false,"given":"Tyler","family":"Sakamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4950-2744","authenticated-orcid":false,"given":"David","family":"Exposito-Alonso","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7898-0227","authenticated-orcid":false,"given":"Janet H. 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