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When the causative genetic mutations are not identified, this opens the possibility of discovering new pathogenic genes or pathways that could be contributing to the condition. In our previous study, we identified a novel candidate pathogenic somatic variant of IRS-1 c.1791dupG in the brain tissue of a child with focal cortical dysplasia type II. This study further explored the variant\u2019s role in causing type II focal cortical dysplasia through in vitro overexpression in 293T and SH-SY5Y cells and in vivo evaluation via in utero electroporation in fetal brains, assessing effects on neuronal migration, morphology, and network integrity. It was found that the mutant IRS-1 variant led to hyperactivity of p-ERK, increased cell volume, and was predominantly associated with the MAPK signaling pathway. In vivo, the IRS-1 c.1791dupG variant induced abnormal neuron migration, cytomegaly, and network hyperexcitability. Notably, the ERK inhibitor GDC-0994, rather than the mTOR inhibitor rapamycin, effectively rescued the neuronal defects. This study directly highlighted the ERK signaling pathway\u2019s role in the pathogenesis of focal cortical dysplasia II and provided a new therapeutic target for cases of focal cortical dysplasia II that are not treatable by rapamycin analogs.<\/jats:p>","DOI":"10.1093\/cercor\/bhae227","type":"journal-article","created":{"date-parts":[[2024,6,5]],"date-time":"2024-06-05T10:56:37Z","timestamp":1717584997000},"source":"Crossref","is-referenced-by-count":3,"title":["Focal cortical dysplasia II caused by brain somatic mutation of <i>IRS-1<\/i> is associated with ERK signaling pathway activation"],"prefix":"10.1093","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0265-3289","authenticated-orcid":false,"given":"Xiao","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Peking University First Hospital , No. 1 Xi\u2019an Men Street, West District, Beijing 100034 , China"},{"name":"Beijing Key Laboratory of Molecular Diagnosis and Study on 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