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Here, we addressed the functional consequences of recurrent cancer\u2010associated\n                    <jats:italic>ERBB4<\/jats:italic>\n                    mutations that are located at regions important for receptor activation and\/or are paralogous to known oncogenic hotspot mutations in other\n                    <jats:italic>ERBB<\/jats:italic>\n                    genes. Eleven out of 18 analyzed mutations were transforming in cell models, thus suggesting oncogenic potential for more than half of the recurrent ERBB4 mutations. More detailed analyses of the most potent mutations, S303F, E452K, and L798R, showed that they are activating, can co\u2010operate with other ERBB receptors and are sensitive to clinically available second\u2010generation pan\u2010ERBB inhibitors neratinib, afatinib, and dacomitinib. Furthermore, the S303F mutation, together with a previously identified activating ERBB4 mutation, E715K, promoted resistance to third\u2010generation EGFR inhibitor osimertinib in EGFR\u2010mutant lung cancer model\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Together, these results are expected to facilitate clinical interpretation of the most recurrent cancer\u2010associated\n                    <jats:italic>ERBB4<\/jats:italic>\n                    mutations. The findings provide rationale for testing the efficacy of clinically used pan\u2010ERBB inhibitors in patients harboring driver\n                    <jats:italic>ERBB4<\/jats:italic>\n                    mutations both in the treatment\u2010na\u00efve setting, and upon development of resistance to targeted agents.\n                  <\/jats:p>","DOI":"10.1002\/1878-0261.70189","type":"journal-article","created":{"date-parts":[[2025,12,24]],"date-time":"2025-12-24T07:41:41Z","timestamp":1766562101000},"page":"1323-1346","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Recurrent cancer\u2010associated\n                    <scp>ERBB4<\/scp>\n                    mutations are transforming and confer resistance to targeted therapies"],"prefix":"10.1002","volume":"20","author":[{"given":"Veera K.","family":"Ojala","sequence":"first","affiliation":[{"name":"Institute of Biomedicine, and MediCity Research Laboratory 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