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Consequently, a greater understanding of the factors regulating cell cycle progression becomes essential to help enhance the response to these new therapies. Here, using data from the Cancer Dependency Map, we identified FAM53C as a new regulator of cell cycle progression. We found that FAM53C is critical for this cell cycle transition and that it acts upstream of the Cyclin D-CDK4\/6-RB axis and of p53 in the regulation of the G1\/S transition. By mass spectrometry, biochemical, and cellular assays, we identified and validated DYRK1A as a cell cycle kinase that is inhibited by and directly interacts with FAM53C. Consistent with the role for FAM53C identified in cells in culture,\n                    <jats:italic>FAM53C<\/jats:italic>\n                    knockout human cortical organoids display increased cell cycle arrest and growth defects.\n                    <jats:italic>Fam53C<\/jats:italic>\n                    knockout mice show minor behavioral phenotypes. Because DYRK1A dysregulation contributes to developmental disorders such as Down syndrome as well as tumorigenesis, future strategies aiming at regulating FAM53C activity may benefit a broad range of patients.\n                  <\/jats:p>","DOI":"10.7554\/elife.109708","type":"journal-article","created":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T14:30:13Z","timestamp":1765463413000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.109708","source":"Crossref","is-referenced-by-count":1,"title":["The FAM53C\/DYRK1A axis regulates the G1\/S transition of the cell cycle"],"prefix":"10.7554","volume":"14","author":[{"given":"Taylar","family":"Hammond","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00f54p054","id-type":"ROR","asserted-by":"publisher"}],"name":"Departments of Pediatrics, Stanford University","place":["Stanford, United States"]},{"id":[{"id":"https:\/\/ror.org\/00f54p054","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of 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