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]. This evidence concerns the gene TKT and chronic myelogenous leukemia, BCR-ABL1 positive.