A 41-year-old male was admitted to our hospital due to fever and purpura. Peripheral blood values were hemoglobin 89 g/L, platelets 16 × 109/L, and white blood cells 3.4 × 109/L with 46% myeloblasts. Bone marrow examination showed hypercellular marrow with 71.0% myeloblasts and 23.0% other myeloid cells. Some of myeloblasts in the peripheral blood and bone marrow had one or two micronuclei (Image 1A, B). Furthermore, many large granules, suggestive of pseudo-Chediak–Higashi granules, were found in the cytoplasm of bone marrow myeloblasts (Image 1C). Dysplastic changes including degranulation and abnormal lobulation were observed in differentiated myeloid cells. Myeloblasts stained positive for myeloperoxidase and chloroacetate esterase. These cells were also positive for CD13, CD33, and HLA-DR, but negative for CD34. G-banding analysis of the bone marrow cells showed 43,X,-Y,-5,add(7)(q22),-20,1∼40dmin[20] (Image 2A, B). Fluorescence in situ hybridization (FISH) with IGH/MYC/CEP 8 probe on metaphase spreads revealed multiple MYC signals on the double minute chromosomes, indicating marked amplification of the MYC gene (Image 2C). In addition, FISH on interphase nuclei confirmed that micronuclei were heavily labeled with the MYC probe in 2 of 100 cells (Image 2D). Taking these hematological and cytogenetic findings into consideration, we made a diagnosis of acute myeloid leukemia (AML) with myelodysplasia-related changes according to the World Health Organization classification, or AML M2 by the French–American–British classification. The patient received two courses of standard induction therapy, but did not achieve complete remission. He underwent allogeneic stem cell transplantation because of worst prognosis cytogenetics including monosomal karyotype 1. Micronuclei are defined as small nucleus-like structures that can be expelled from the nucleus. They usually contain amplified oncogenes, acentric chromosomal fragments, or whole damaged chromosomes 2. Double minute chromosomes (dmin) are small chromatin bodies that lack centromeres and frequently mediate oncogene amplification in human tumors, although they are rarely found in AML. These chromosomes are commonly correlated with amplification of MYC at 8q24 or less commonly MLL at 11q23 3-5. The presence of dmin as part of complex karyotypes in AML appears to bring about chemotherapy resistance and rapid progression of the disease. To our knowledge, the association between micronuclei in myeloblasts and dmin with MYC amplification has previously been demonstrated in only one study 2. In the present case, it is confirmed that dmin on metaphase cells and micronuclei on interphase cells also contained markedly amplified MYC. On the other hand, pseudo-Chediak–Higashi granules, which are formed by fusion of azurophilic granules and show myeloperoxidase activity, are occasionally found in AML with or without dmin 6. They were also detected in two of four AML cases with micronuclei and MYC amplification 2. Thus, simultaneous detection of cytoplasmic micronuclei and pseudo-Chediak–Higashi granules in myeloblasts may imply cytogenetic abnormalities including dmin, and eventually predict poor prognosis on initial diagnosis of AML.