Dear Editor, The coexistence of chronic myelogenous leukemia (CML) and multiple myeloma (MM) is an extremely rare event [1]. Imatinib mesylate (IM) has become the mainstay first line treatment for CML [2]. We report the case of a patient who was diagnosed with CML and developed MM after 10 months of treatment with IM. To our knowledge, our patient is the third case of CML preceding the occurrence of MM and the second case of occurrence of MM post IM treatment for CML [3]. A 76-year-old white male was diagnosed with CML in May 2003. Cytogenetic analysis revealed the presence of Philadelphia (Ph) chromosome: 46 XY, t(9;22) (q34;q11). BCR/ABL mRNA transcript was detected by reverse transcription polymerase chain reaction (RT-PCR). Interphase fluorescence in-situ hybridization (iFISH) in bone marrow smears revealed deletion of the 5′ ABL on the derivative chromosome 9 in 62% of the cells. The patient received interferon-alpha. Treatment with interferon was switched to IM (400 mg once daily) after 4 months because of severe side effects as whole body worsening erythema and pruritus related to interferon. Bone marrow aspirate, 10 months after the initiation of imatinib treatment, showed normal cellularity, white and red lineages decreased and a plasma cell count of 60%. Cytogenetic analysis showed no cytogenetic response. A new iFISH in bone marrow revealed again the deletion of the 5′ ABL on the derivative chromosome 9 in 28% of the cells and trisomy 9 in 49% of the cells. Laboratory tests showed anemia, but a skeletal survey showed no lytic lesions. Serum immunofixation demonstrated an IgA κ-type chain M-protein (19.5 g/l) without depression of the other immunoglobulins and k light chains 1,700 mg/dl. Bone marrow biopsy disclosed diffuse bone marrow infiltration by plasma cells, which were k light chain positive with immunoperoxidase staining. iFISH on plasma cells showed no rearrangement involving IGH gene, 13qor p53 but trisomy of one, three and seven chromosomes in all plasma cells, indicating a hyperdiploid MM. The patient’s clinical condition deteriorated and he was dependent on red blood cell transfusion. He was treated with melphalan and prednisolone; imatinib was continued. Six months later, a bone marrow aspirate showed normal findings with a plasma cell count of 3%. No M-protein was detectable on serum immunofixation. iFISH study showed 97% of the marrow cells to be BCR/ABLpositive but it failed to reveal any aneuploid cells. Six months later, the patient progressed to blast crisis and died because of massive bleeding from the upper gastrointestinal tract. Our patient developed MM 10 months post IM treatment, but it is difficult to prove whether the development of MM was random or accelerated by IM. It is reported that IM has inhibited the proliferation of MM cells by arresting cell cycle progression and furthermore inhibited the proliferation of MM cells resistant to dexamethasone or melphalan and had an Ann Hematol (2009) 88:281–282 DOI 10.1007/s00277-008-0597-2