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This review provides a comprehensive overview of the current molecular landscape of MF beyond canonical driver mutations (\n                      <jats:italic>JAK2<\/jats:italic>\n                      ,\n                      <jats:italic>MPL or CALR)<\/jats:italic>\n                      , emphasizing insights gained from murine models that served as valuable tools for understanding disease mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Findings<\/jats:title>\n                    <jats:p>\n                      High-throughput next-generation sequencing (NGS) has markedly enhanced our understanding of the molecular basis of MF, identifying numerous mutations beyond the canonical driver genes\n                      <jats:italic>JAK2<\/jats:italic>\n                      ,\n                      <jats:italic>MPL<\/jats:italic>\n                      , and\n                      <jats:italic>CALR<\/jats:italic>\n                      , which are present in about 80% of patients. Additional mutations affect genes involved in DNA methylation (\n                      <jats:italic>TET2<\/jats:italic>\n                      ,\n                      <jats:italic>DNMT3A<\/jats:italic>\n                      ,\n                      <jats:italic>IDH1<\/jats:italic>\n                      ,\n                      <jats:italic>IDH2<\/jats:italic>\n                      ), histone modification (\n                      <jats:italic>ASXL1<\/jats:italic>\n                      ,\n                      <jats:italic>EZH2<\/jats:italic>\n                      ), mRNA splicing (\n                      <jats:italic>SF3B1<\/jats:italic>\n                      ,\n                      <jats:italic>SRSF2<\/jats:italic>\n                      ,\n                      <jats:italic>U2AF1<\/jats:italic>\n                      ,\n                      <jats:italic>ZRSR2<\/jats:italic>\n                      ), signaling pathways (\n                      <jats:italic>CBL<\/jats:italic>\n                      ,\n                      <jats:italic>NRAS<\/jats:italic>\n                      ,\n                      <jats:italic>KRAS<\/jats:italic>\n                      ), and key transcription factors (\n                      <jats:italic>RUNX1<\/jats:italic>\n                      ,\n                      <jats:italic>NFE2<\/jats:italic>\n                      ,\n                      <jats:italic>TP53<\/jats:italic>\n                      ). The presence and combination of these alterations influence clinical presentation, prognosis, and therapeutic response.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary<\/jats:title>\n                    <jats:p>This review offers an updated synthesis of the evolving molecular landscape of MF, highlighting how the intricate interplay among genetic alterations has deepened our understanding of disease heterogeneity, allowing refined risk stratification and therapeutic planning. Advances emerging from molecular research and experimental models are progressively translating into clinical practice, promoting more personalized and targeted approaches to the management of MF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11899-026-00773-6","type":"journal-article","created":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T06:32:23Z","timestamp":1770705143000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The Role and Impact of Non-driver Gene Mutations in Myelofibrosis"],"prefix":"10.1007","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5463-4736","authenticated-orcid":false,"given":"Valentina","family":"Boldrini","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paola","family":"Guglielmelli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandro M.","family":"Vannucchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,10]]},"reference":[{"issue":"11","key":"773_CR1","first-page":"1200","volume":"140","author":"DA Arber","year":"2022","unstructured":"Arber DA, et al. 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