An 18-month-old boy was consulted to a pediatric clinic with a 5-month history of purpuric macules and nodules on the scalp. He had a history of trauma (falling down from a chair) to the scalp about 6 months before the consultation. He had been brought to an emergency department after the trauma. Cranial computed tomography revealed a small crack on the temporal bone. Purpuric macules and nodules of the scalp had been noticed on the control 1 month later. Results of total blood tests had been within normal limits. Dermatologic examination disclosed multiple pink to violaceous infiltrated cutaneous nodules and purpuric macules with diameters of0.5 to 1.5 cm on his scalp (Figure 1). No petechiae or ecchymoses were seen. Cervical lymphadenopathy was detected during physical examination. There was no hepatosplenomegaly. A punch biopsy was obtained from one of the infiltrated nodules and was sent for histopathologic examination. Histopathologic examination revealed diffuse dermal and subcutaneous edema, erythrocyte extravasation and infiltration by monomorphic cells with large hyperchromatic nuclei, and high mitotic activity (Figure 2). Histopathologic staining was positive for leukocyte common antigen and CD68 in these cells. Results of complete blood cell count of the patient were as follows: hemoglobin: 8.44 g/dL; white blood cell count: 29.2 x 10(9)/L; and platelet count 55.6 x 10(9)/L. Bone marrow aspirate results showed 68.4% blast cells and a biopsy specimen confirmed the diagnosis of acute myeloid leukemia, with flow cytometry findings positive for acute monoblastic leukemia (AML) French-American-British (FAB)-M5 phenotype. We initiated induction chemotherapy for AML (AML-M5) according to the AML Berlin-Frankfurt-Munster 2004 protocol.' Complete resolution of the leukemia cutis lesions was attained with chemotherapy at the end of the first month of treatment.