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Detection of <jats:italic>JAK2<\/jats:italic> fusion genes is important as patients with aberrantly activated JAK2 may benefit from treatment with tyrosine kinase inhibitors such as ruxolitinib. Here, we report a novel fusion gene between the transcriptional co\u2010repressor\u2010encoding gene transducin\u2010like enhancer of split 3 (<jats:italic>TLE3)<\/jats:italic> and <jats:italic>JAK2<\/jats:italic> in a patient initially diagnosed with chronic eosinophilic leukemia with additional mutations in <jats:italic>PTPN11<\/jats:italic> and <jats:italic>NRAS<\/jats:italic>. The patient was successfully treated with the JAK2 inhibitor ruxolitinib for 8\u2009months before additional somatic mutations were acquired and the disease progressed into an acute lymphoblastic T\u2010cell leukemia\/lymphoma. The present case shows similarities to previously reported cases with <jats:italic>PCM1::JAK2<\/jats:italic> and <jats:italic>BCR::JAK2<\/jats:italic> with regard to disease phenotype and response to ruxolitinib, and importantly, provides an example that also patients harboring other <jats:italic>JAK2<\/jats:italic> fusion genes may benefit from treatment with JAK2 inhibitors.<\/jats:p>","DOI":"10.1002\/gcc.23261","type":"journal-article","created":{"date-parts":[[2024,8,6]],"date-time":"2024-08-06T13:25:54Z","timestamp":1722950754000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp><i>TLE3<\/i><\/scp> Is a Novel Fusion Partner of <scp><i>JAK2<\/i><\/scp> in Myeloid\/Lymphoid Neoplasm With Eosinophilia Responding to <scp>JAK2<\/scp> 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