Case Reports in Hematology a large epidemiological study to speciﬁcally assess the risk of developing second primary CML after chemotherapy and/or radiotherapy is stressed. Another question that might still be in our mind is that, whether the results of Philadelphia chromosome cytogenetic analysis and molecular diagnosis of BCR-ABL had been underestimated due to technical defect at diagnosis and patient was actually Ph(+) ALL and had been misdiagnosed at ﬁrst, but from the fact that Ph(+) ALL patients have a poor prognosis and the 5-year event-free survival (EFS) ranges from 10% to 20%, in Ph(+), versus 76% in the Ph(−) pop- ulation and recurrent disease in these patients is mainly due to failure of treatment, and the poor prognosis persists even after stratiﬁcation in a high-risk treatment protocol [7]. In our case due to the good response to prednisolone and being on conventional BFM protocol and completing the protocol without any complications and 3 years of disease free survival actually conﬁrms Ph(−) ALL with a favorable prognosis. 4. Conclusion This case may be the ﬁrst case ever reported with such a unique presentation, which indicates strongly the need for long-term followup of patients, and, due to a history of Ph(−) pre-B-ALL and by the fact that CML is a molecular disease, to wait and watch, whether the natural history of CML molecular behavior is changed by the time and whether in this case whose patient had been taking imatinib (BCR-ABL tyrosine kinase inhibitor) since CML diagnosis, the appearance and persistence of cytogenetically abnormal Ph(−) clone arising in the context of imatinib-induced major molecular response is sustained or there might be some clonal progression and imatinib resistance in the future. Another important point in this case is to follow up patient in the future and to see whether depletion of Ph(+) stem cells make hematopoesis dependent on Ph(−) stem cells, in theory nonmalignant, and eventually clonal changes of the MDS type or of acute leukemia may appear which may be representative of a preleukemic stage of Ph(−) CML with some level of genetic instability. References [1] P. J. Fialkow, R. J. Jacobson, and T. Papayannopoulou, “Chronic myelocytic leukemia: clonal origin in a stem cell common to the granulocyte, erythrocyte, platelet and monocyte/macrophage,” American Journal of Medicine, vol. 63, no. 1, pp. 125–130, 1977. [2] R. E. Champlin and D. W. Golde, “Chronic myelogenous leukemia: recent advances,” Blood, vol. 65, no. 5, pp. 1039–1040, 1985. [3] C. D. Bloomﬁeld, A. I. Goldman, G Alimena et al., “Chromoso- mal abnormalities identify high-risk and low-risk patients with acute lymphoblastic leukemia,” Blood, vol. 67, no. 2, pp. 415– 420, 1986. [4] M. Schrappe, M. Arico` , J. Harbott et al., “Philadelphia chromosome-positive (Ph+) childhood acute lymphoblastic leukemia: good initial steroid response allows early prediction of a favorable treatment outcome,” Blood, vol. 92, no. 8, pp. 2730–2741, 1998. 3 [5] C. A. Westbrook, A. L. Hooberman, C. Spino et al., “Clinical signiﬁcance of the BCR-ABL fusion gene in adult acute lymphoblastic leukemia: a cancer and leukemia group B study,” Blood, vol. 80, no. 12, pp. 2983–2990, 1992. [6] R. Kurzrock, J. U. Gutterman, and M. Talpaz, “The molecular genetics of Philadelphia chromosome-positive leukemias,” New England Journal of Medicine, vol. 319, no. 15, pp. 990–998, 1988. [7] H. Espe´rou, J.-M. Boiron, J.-M. Cayuela et al., “A poten- tial graft-versus-leukemia eﬀect after allogeneic hematopoi- etic stem cell transplantation for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia: results from the French Bone Marrow Transplantation Society,” Bone Marrow Transplantation, vol. 31, no. 10, pp. 909–918, 2003. [8] M. G. vaz de Campos, M. L. L. Ferrari Chauﬀaille, C. Arrais Rodrigues, E. A. Krum, and M. Yamamoto, “A rare case of Acute Lymphocytic Leukemia (ALL) presenting with double Philadelphia chromosome—relapse or secondary leukemia,” Genetics and Molecular Biology, vol. 26, no. 3, pp. 249–251, 2003. [9] S. Faderl, M. Talpaz, Z. Estrov, S. O’Brien, R. Kurzrock, and H. M. Kantarjian, “The biology of chronic myeloid leukemia,” New England Journal of Medicine, vol. 341, no. 3, pp. 164–172, 1999.