Dear Editor, ABL1 deletion without BCR/ABL1 rearrangement is a rare genetic abnormality [1–3], while ABL1 deletion associated with BCR/ABL1 has occasionally been reported in CML [4, 5]. We previously described a case showing ABL1 deletion without BCR/ABL1 by interphase FISH [3]. Its significance is still to be discovered. Therefore, we performed single nucleotide polymorphism arrays (SNP-A)-based karyotyping, using the specimen obtained from that patient. As previously described, this patient was a 37-year-old man diagnosed as having precursor B cell lymphoblastic leukemia (B-ALL). Cytogenetic analysis showed 65% of metaphase cells bearing add(9)(p22) and add(16)(p13.3). By FISH, ABL1 gene deletion was observed in 76% of interphase cells and ETV6 rearrangement in 81% of cells. Genome-Wide Human SNP 6.0 Array (Affymetrix, CA, USA) was performed per the manufacturer’s instructions, and then analyzed using Genotyping Console v 3.0 (Affymetrix, CA). By SNP-A, 9q deletion (9q12–q34.13, 64 Mb) and two regions of 20q deletion (20q13.13–q13.13, 0.9 Mb; 20q13.2–q13.32, 1.5 Mb) were observed (Fig. 1). This finding indicated that an ABL1 deletion identified by FISH was, in fact, a part of large-sized 9q deletion, rather than just a monoallelic loss of ABL1 gene, leading to haploinsufficiency of more than 100 genes in that region. The size of 9q deletion observed in this case was large enough to be identified by metaphase cytogenetics. However, those regions could be detected only by techniques using interphase cells, suggesting that the leukemic cells bearing 9q deletion did not actively divide. Similar to our case, array CGH confirmed a large-sized 9q deletion (9q22.33–q34.3, 38 Mb) in a B-ALL patient with ABL1 deletion not associated with BCR/ABL1 rearrangement identified by interphase FISH [4]. The other study using array CGH also demonstrated that in 20% of patients with normal karyotype B-ALL, 9q deletions covered larger genomic distances (8–12Mb)[6]. Taken together, the 9q deletion may result in the loss of multiple tumor suppressor gene(s) that contribute to B-ALL pathogenesis, although the target genes remain unknown. Further studies to clarify its potential effect of large sized 9q deletion are needed. On the other hand, a monogenic SET/NUP214 fusion gene caused by a submicroscopic 9q34 deletion has been reported in T-cell ALL or AML [7–10]. In one study using array CGH, a 9q deletion (9q34.11–q34.13, 3 Mb) in BALL resulted in a formation of fusion gene from the juxtaposition of the telomere region of the SET gene with NUP214 [6]. Accordingly, it is likely that a submicroscopic 9q34 deletion results in the SET/NUP214 rearrangement, while the role of 9q deletion covering larger genomic lesions remains to be cleared. This study was supported by a grant (2009) from Mokdong Hospital, Ewha Womans University School of Medicine