Structural variants (SV) that give rise to tyrosine kinase (TK) fusion genes are seen recurrently in myeloid neoplasms, specifically chronic myeloid leukaemia (CML), which is defined by the presence of BCR::ABL1, but also in the much less common entity “myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions” (MLN-TK), characterized by rearrangements of PDGFRA, PDGFRB, FGFR1, JAK2, FLT3, ETV6::ABL1 and other TK fusions [1, 2]. The gene discussed is FLT3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.