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Therefore, it is not surprising that aberrant activation of<jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>is associated with developmental malformations and epileptogenesis. A broad spectrum of malformations of cortical development, such as focal cortical dysplasia (<jats:styled-content style=\"fixed-case\">FCD<\/jats:styled-content>) and tuberous sclerosis complex (<jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>), have been linked to either germline or somatic mutations in<jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>pathway\u2010related genes, commonly summarised under the umbrella term \u2018<jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>opathies\u2019. However, there are still a number of unanswered questions regarding the involvement of<jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>in the pathophysiology of these abnormalities. Therefore, a monogenetic disease, such as<jats:styled-content style=\"fixed-case\">TSC<\/jats:styled-content>, can be more easily applied as a model to study the mechanisms of epileptogenesis and identify potential new targets of therapy. Developmental neuropathology and genetics demonstrate that<jats:styled-content style=\"fixed-case\">FCD II<\/jats:styled-content>b and hemimegalencephaly are the same diseases. Constitutive activation of<jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>signalling represents a shared pathogenic mechanism in a group of developmental malformations that have histopathological and clinical features in common, such as epilepsy, autism and other comorbidities. We seek to understand the effect of<jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>dysregulation in a developing cortex with the propensity to generate seizures as well as the aftermath of the surrounding environment, including the white matter.<\/jats:p>","DOI":"10.1111\/joa.12956","type":"journal-article","created":{"date-parts":[[2019,3,22]],"date-time":"2019-03-22T14:38:34Z","timestamp":1553265514000},"page":"521-542","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":96,"title":["New insights into a spectrum of developmental malformations related to<scp>mTOR<\/scp>dysregulations: challenges and perspectives"],"prefix":"10.1111","volume":"235","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9102-7353","authenticated-orcid":false,"given":"A.","family":"M\u00fchlebner","sequence":"first","affiliation":[{"name":"Department of Neuropathology Amsterdam UMC University of Amsterdam Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Bongaarts","sequence":"additional","affiliation":[{"name":"Department of Neuropathology Amsterdam UMC University of Amsterdam Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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