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However, the precise role of NSD2 in brain development remains unclear. Here, we identify NSD2 as a pivotal epigenetic regulator orchestrating the transition from neurogenesis to gliogenesis in the developing mouse neocortex. Conditional knockout of\n                    <jats:italic>Nsd2<\/jats:italic>\n                    severely impairs astrocyte production in late embryogenesis, while its overexpression promotes astrocytic fate. Integrated epigenomic and transcriptomic analyses reveal that NSD2 deposits the activating histone mark H3K36me2 directly at the\n                    <jats:italic>Egfr<\/jats:italic>\n                    promoter, sustaining EGFR expression and downstream ERK signaling\u2014a pathway essential for gliogenesis. Pharmacological activation of ERK phosphorylation rescues the astrogliogenesis defects both in vitro and in vivo. Notably,\n                    <jats:italic>Nsd2<\/jats:italic>\n                    \u2010deficient mice exhibit significant deficits in learning and memory. Our findings define an NSD2\u2010H3K36me2\u2010EGFR\u2010ERK axis that drives cortical gliogenesis and provide mechanistic insights into the potential contribution of NSD2 deficiency to neurodevelopmental abnormalities.\n                  <\/jats:p>","DOI":"10.1002\/advs.76695","type":"journal-article","created":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T12:46:08Z","timestamp":1785156368000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["NSD2 Coordinates the Neurogenic\u2010to\u2010Gliogenic Transition via H3K36me2\u2010Dependent Activation of the EGFR\u2010ERK Pathway"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-4044-8475","authenticated-orcid":false,"given":"Hanxue","family":"Chen","sequence":"first","affiliation":[{"name":"State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry &amp; Molecular Biology, Institute of Basic 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