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Patients exhibit microcephaly, micrognathia, malar hypoplasia, external ear anomalies, eye anomalies, psychomotor delay, intellectual disability, limb, and heart defects. Craniofacial malformations in these patients are predominantly found in neural crest cells\u2010derived structures of the face and head. Mutations in eight genes\n                    <jats:italic>SNRPB<\/jats:italic>\n                    ,\n                    <jats:italic>RNU4ATAC<\/jats:italic>\n                    ,\n                    <jats:italic>SF3B4<\/jats:italic>\n                    ,\n                    <jats:italic>PUF60<\/jats:italic>\n                    ,\n                    <jats:italic>EFTUD2<\/jats:italic>\n                    ,\n                    <jats:italic>TXNL4<\/jats:italic>\n                    ,\n                    <jats:italic>EIF4A3<\/jats:italic>\n                    , and\n                    <jats:italic>CWC27<\/jats:italic>\n                    are associated with craniofacial spliceosomopathies. In this review, we provide a brief description of the normal development of the head and the face and an overview of mutations identified in genes associated with craniofacial spliceosomopathies. We also describe a model to explain how and when these mutations are most likely to impact neural crest cells. We speculate that mutations in a subset of core splicing factors lead to disrupted splicing in neural crest cells because these cells have increased sensitivity to inefficient splicing. Hence, disruption in splicing likely activates a cellular stress response that includes increased skipping of regulatory exons in genes such as\n                    <jats:italic>MDM2<\/jats:italic>\n                    and\n                    <jats:italic>MDM4<\/jats:italic>\n                    , key regulators of P53. This would result in P53\u2010associated death of neural crest cells and consequently craniofacial malformations associated with spliceosomopathies.\n                  <\/jats:p>","DOI":"10.1002\/dvdy.183","type":"journal-article","created":{"date-parts":[[2020,4,21]],"date-time":"2020-04-21T14:01:02Z","timestamp":1587477662000},"page":"924-945","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":66,"title":["Spliceosomopathies and neurocristopathies: Two sides of the same coin?"],"prefix":"10.1002","volume":"249","author":[{"given":"Marie\u2010Claude","family":"Beauchamp","sequence":"first","affiliation":[{"name":"Department of Pediatrics McGill University  Montreal Quebec Canada"},{"name":"McGill University Health Centre at Glen Site  Montreal Quebec Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabrina Shameen","family":"Alam","sequence":"additional","affiliation":[{"name":"McGill University Health 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