We have read with great interest but also astonishment, the publication by Gmidene et al. regarding the deletion of chromosomal region 8p21.3 in multiple myeloma (MM) patients [1]. While this study claims to be the first to present the deletion of this region in MM patients, we would like to draw attention to previous work in the field published by us and others. In the January 2009 issue of the British Journal of Haematology, we have presented our observations on the deletion of the 8p21 region and the prognostic significance it presents [2]. Using a commercially available FISH probe located on the 8p21 region, we have identified that 14/58 patients tested (24 %) carried this deletion at the time of diagnosis. In 2010, a larger study by Neben et al. has evaluated 236 MM patients and reported a 19 % frequency for this cytogenetic abnormality [3]. Although using a smaller group of patients, the study by Gmidene et al. describes a similar frequency of the deletion: 21.6 % (8/37 patients) that falls in line with the two previously published observations. Although there are minor differences in the FISH probes used for analysis in these three studies, the similarity of frequencies reported strongly suggests that a similar group of patients are identified with the different approaches. The study by Gmidene et al. confirms our previous report and taken altogether with Neben et al., these data convincingly demonstrate that del(8)(p21) is seen in about 1/5 of MM patients. We have also reported that del(8)(p21) stands out as a significant factor for poor prognosis in MM patients receiving autologous stem cell transplantation [2]. Survival analysis has revealed that loss of8p21 wassignificantlyassociated with poor progression-free survival (PFS: 12 vs. 27 months in patients without the deletion, p \0.05) and overall survival (OS: 24 vs. 67 months in patients without the deletion, p\ 0.005). Moreover, in this group of patients, multivariate analysis of prognostic factors has also identified del(8)(p21) as an independent prognosticfactorforbothPFS(p = 0.033)andOS(p = 0.029). Similarly, Neben et al. have also identified del(8)(p21) as a statistically significant prognostic factor for both PFS (p = 0.011) and OS (p = 0.040), while this significance was lost after p values were adjusted for ISS criteria[3]. In multivariate analysis, del(8)(p21) did not present as an independent factor, possibly due to the use of a larger number of variables compared to our study as well as differences in treatment regimens. Unfortunately, the current study by Gmidene et al. does not present any survival data on the reported patients. Regarding the correlation of the occurrence of different chromosomalaberrations, thehierarchicalclusteringanalysis in our study has presented a very close link between del(8)(p21) and t(4;14), while the correlations with del(17)(p13) and del(13)(q14)weresomewhatweaker.Nebenetal.havereported a significant correlation with del(13)(q14) (p = 0.04) and the absence of correlation with the occurrence of amp1(q)(21) (p = 0.06). Confirming the previous work, Gmidene et al. also suggest a link of del(8)(p21) with del(13)(q14) and t(4;14). In our 2009 paper as well as a review on chromosomal aberrations in MM that was published in 2010 [4], we have drawn attention to the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor gene cluster located in this locus and hypothesized that the downregulation of TRAIL receptor expression due to del(8)(p21) might cause decreased sensitivity of tumor cells to TRAIL-mediated apoptosis [5], providing an advantage for immune escape of the malignant clone [6]. In a similarly structured discussion, Gmidene et al. also speculate about the possibility of such a phenomenon resulting from the deletion of TRAIL receptor T. Sutlu E. Alici G. Gahrton (&) H. Nahi Department of Medicine, M54, Karolinska Institutet, Center for Hematology and Regenerative Medicine, Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden e-mail: gosta.gahrton@ki.se