We read with great interest ‘‘Coexistence of inversion 16 and the Philadelphia chromosome comprising P190 BCR/ ABL in chronic myeloid leukemia blast crisis’’ by Ninomiya et al. [1]. As the authors note, their case represents the first reported usage of the minor BCR breakpoint in the setting of chronic myelogenous leukemia (CML) in myeloid blast phase with a concomitant inv(16)(p13.1q22). All previously investigated similar cases show usage of the major BCR breakpoint, while all investigated cases of de novo acute myeloid leukemia (AML) with coexisting inv(16)(p13.1q22) and t(9;22)(q34;q11.2) use the minor BCR breakpoint. Indeed, this pattern is reinforced by several patients described in the literature but not listed in the authors’ Table 1 ‘‘Summary of reported cases of Ph? myeloid leukemia with inv(16)’’ [2–4]. In addition, we have recently seen a patient who conforms to this apparent pattern. A 49-year-old woman developed persistent leukopenia (white blood cell count 1.7 9 10/L) and mild thrombocytopenia (platelet count 113 9 10/L) 12 months after the initiation of therapy for infiltrating ductal carcinoma of the breast. Her treatment regimen had included four cycles of adriamycin and cyclophosphamide, followed by paclitaxel and trastuzumab. She had also undergone a bilateral mastectomy, and radiation therapy to the chest wall had been initiated 8 months after her original diagnosis. Other than the leukopenia and thrombocytopenia, her CBC parameters were unremarkable. There were no physical or symptomatic findings of note. Review of the peripheral blood smear identified rare circulating blasts (1–2%) with fine chromatin, irregular nuclear contours and conspicuous nucleoli. A bone marrow evaluation revealed hypercellularity with increased blasts (10–15%) and abnormal eosinophils with basophilic granules. By flow cytometric analysis, the blasts showed a myeloid immunophenotype (positive for CD13, dim CD33, HLADR, CD117, and myeloperoxidase; negative for CD2, surface CD3, CD4, CD5, CD8, CD10, CD19, CD20, TdT, CD64, CD14, and CD34). Cytogenetic analysis revealed a karyotype of 46,XX,inv(16)(p13.1q22)[5]/46,idem,t(9;22)(q34;q11.2) [7]/46,XX[8], and fluorescence in situ hybridization confirmed the CBFB (16q22) rearrangement. Thus, both the inv(16) and the Philadelphia chromosome were present in the same metaphase cells, and did not represent biclonal populations. RT-PCR analysis revealed e1-a2 BCR-ABL1 transcripts, corresponding to the p190 minor form, but no e13-a2 or e14-a2 (p210, major form) transcripts (Figs. 1, 2, 3). Given the patient’s history, our diagnosis was therapy-related myeloid neoplasm. The overall findings, including the usage of the minor BCR breakpoint, correlate well with the previously documented pattern of de novo AML with coexisting inv(16)(p13.1q22) and t(9;22)(q34;q11.2). The present case is the second reported therapy-related myeloid neoplasm with coexisting inv(16) and t(9;22), and is similar in many respects to the previously described case [2]. Somewhat remarkably, our patient showed no evidence of the BCR-ABL1 fusion by FISH or RT-PCR after only 3 weeks of single agent treatment with imatinib mesylate. Thus, including our patient, there appear to be at least 18 patients described in the literature with simultaneous D. Bustamante (&) D. R. Czuchlewski Department of Pathology, University of New Mexico, TriCore Reference Laboratories, 1001 Woodward Place NE, Albuquerque, NM 87102, USA e-mail: DCzuchlewski@salud.unm.edu