Dear Editor, We report a case of a 61-year-old woman with a prior history of hypertension, dyslipidemia, and ischemic cardiopathy who was admitted to our hospital complaining of dyspnea and cardiopalmus. Physical examination and laboratory tests including HIV serology and lactate dehydrogenase (LDH) were normal. Transthoracic echocardiography demonstrated a large mass arising from the right ventricle with associated pericardial and pleural effusions. Magnetic resonance imaging scans displayed also an involvement of the tricuspidal valve with secondary stenosis and complete infiltration of the ventricular wall. The patient underwent exploratory thoracotomy that revealed a mass extending from the atrium to the ventricle and impairing diastolic filling. This mass was almost completely excised. Histological section disclosed a Burkitt’s Non-Hodgkin’s Lymphoma: tumor consisted of small round cleaved cell with small nuclei surrounded by a deeply basophilic cytoplasm and admixed starry-sky histiocytes. Immunohistochemical examinations showed positivity of lymphoma cells for CD20, IgM, bcl6, CD10, Ki67 100% (EBV-; see Fig. 1a,c,b,d). A total body computed tomography (CT) scan did not demonstrate any lymph node enlargement or visceral involvement. Bone marrow cytology and histology showed a focal, minimal infiltration by lymphoma cells. After a short rehabilitation program, the patient was treated with a pre-phase of high-dose Dexametasone. During this phase, an epigastric palpable mass appeared, and an EGDS showed a thickening of the gastric wall due to lymphoma localization as showed by biopsy. A PET/CT scan demonstrated moreover an elevated pathological uptake of stomach, duodenum, omentum, retroperitoneal lymph nodes, pelvic bone, femur, and vertebral column. A second examination of bone marrow cytology at that time demonstrated 100% infiltration by blasts consistent with classical Burkitt’s Non-Hodgkin’s Lymphoma (BL) in both morphology and immunophenotype. After G-banding and fluorescence in situ hybridization (FISH) analyses, the karyotype was 49, XX, +X, t(8;14)(q24;q32), −14, +der(14)(3;8;14) (q27;q24;q32), +18, +20 (see Fig. 1d). In spite of Dexametasone administration, LDH level markedly increased. The patient started hyper-CVAD regimen, but she died before completing the first cycle. Incidence of cardiac neoplasia is very low, and lymphoproliferative disorders account for about 1% of the primary tumors of heart [1]. Primary cardiac BL has been reported very rarely [2, 3] both in immunocompetent and immunocompromised patients and is associated with a very unfavorable outcome. However, these reports frequently lack complete cytogenetic data fulfilling WHO criteria. Sporadic variants of BL and Burkitt-like lymphoma (BLL) present secondary genomic aberrations more frequently than endemic BL, which could explain their worse prognosis. To our knowledge, only two further cases of Burkitt’s lymphoma have been reported [4, 5] sharing cytogenetic abnormality Ann Hematol (2008) 87:487–488 DOI 10.1007/s00277-007-0414-3