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Advances in molecular genetics and understanding the neurodevelopmental pathogenesis of the epilepsy\u2013autism phenotype may lead to mechanism\u2010based treatments for children with DEEs and autism. Several genes, including the newly reported <jats:italic>PPFIA3<\/jats:italic>, <jats:italic>MYCBP2<\/jats:italic>, <jats:italic>DHX9<\/jats:italic>, <jats:italic>TMEM63B<\/jats:italic>, and <jats:italic>RELN<\/jats:italic>, are linked to various neurodevelopmental and epileptic disorders, intellectual disabilities, and autistic features. These findings underscore the clinical heterogeneity of genetic DEEs and suggest diverse neurobiological mechanisms influenced by genetic, epigenetic, and environmental factors. Mechanisms linking epilepsy and autism include \u03b3\u2010aminobutyric acidergic (GABAergic) signaling dysregulation, synaptic plasticity, disrupted functional connectivity, and neuroinflammatory responses. GABA system abnormalities, critical for inhibitory neurotransmission, contribute to both conditions. Dysregulation of the mechanistic target of rapamycin (mTOR) pathway and neuroinflammation are also pivotal, affecting seizure generation, drug resistance, and neuropsychiatric comorbidities. Abnormal synaptic function and connectivity further underscore the epilepsy\u2013autism phenotype. New treatment options targeting specific mechanisms linked to the epilepsy\u2013autism phenotype are emerging. Genetic variants in potassium channel genes like <jats:italic>KCNQ2<\/jats:italic> and <jats:italic>KCNT1<\/jats:italic> are frequent causes of early onset DEEs. Personalized treatments like retigabine and quinidine have been explored with heterogeneous responses. Efforts are ongoing to develop more effective <jats:italic>KCNQ<\/jats:italic> activators and <jats:italic>KCNT1<\/jats:italic> blockers. <jats:italic>SCN1A<\/jats:italic> genetic variants, particularly in Dravet syndrome, show potential for treatment of autistic symptoms with low\u2010dose clonazepam, fenfluramine, and cannabidiol, although human trials have yet to consistently replicate animal model successes. Early intervention before the age of 3\u2009years, particularly in <jats:italic>SCN1A<\/jats:italic>\u2010 and tuberous sclerosis complex\u2010related DEEs, is crucial. Additionally, targeting the mTOR pathway shows promise for seizure control and managing epilepsy\u2010associated comorbidities. Understanding the distinct autism spectrum disorder phenotype in DEEs and implementing early behavioral interventions are essential for improving outcomes. Despite genetic advances, significant challenges persist in diagnosing and treating DEE\u2010associated epilepsy\u2013autism phenotypes. Future clinical trials should adopt precision health approaches to improve neurodevelopmental outcomes.<\/jats:p>","DOI":"10.1111\/epi.18209","type":"journal-article","created":{"date-parts":[[2025,2,22]],"date-time":"2025-02-22T15:14:21Z","timestamp":1740237261000},"page":"970-987","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["The epilepsy\u2013autism phenotype associated with developmental and epileptic encephalopathies: New mechanism\u2010based therapeutic options"],"prefix":"10.1111","volume":"66","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8120-0287","authenticated-orcid":false,"given":"Nicola","family":"Specchio","sequence":"first","affiliation":[{"name":"Neurology Epilepsy and Movement Disorders Unit, Bambino Ges\u00f9 Children's Hospital Istituti di Ricovero e Cura a Carattere Scientifico, full member of EpiCARE  Rome Italy"},{"name":"University Hospitals KU Leuven  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