The expression of CD56 antigen is associated with poor prognosis in patients with acute myeloid leukemia Our results demonstrated that the OS was significantly lower in the group expressing CD56 in leukemic blasts, which was compatible with published data.(13,16,22) Ferrara et al. demonstrated in a multivariate analysis that CD56 expression is an independent factor for low survival of AML subtype FAB M3 patients.(23) This same difference was observed in another study, which included all AML subtypes with the exception of AML M3 due to its different biology.(13) In our study a higher proportion of CD56 expression was found in men (7:1) compared with the control group (1.2:1) but without significant difference, which confirmed published data.(15,23,28) Only one study reported a higher incidence in male patients with myeloid/NK AL.(24) The incidence of CD56 expression in the patients assessed in our study was 16.7%, similar to rates found in the literature which range from 14 to 58% of AML patients.(13-16,23,29,30) The incidence of FAB subtypes of our patients evidenced a higher proportion in AML FAB M4 cases (37.5%) and FAB M5 cases (25.0%), which were compatible with those reported in literature.(13,16) Raspadori et al.(22) found that CD56 expression was detected more in M2 and M5 patients. The death rate during chemotherapy induction was assessed in our study in order to verify whether the group expressing CD56 had a tendency to higher susceptibility to death; here this did not reach a statistically significant difference which may be attributed to the small study population. None of the authors referenced reported death rates in the induction of chemotherapy, nor did they assess any possible correlation with the CD56 expression. Studies about the prognostic value of CD56 expression in AML are relatively recent and a number of clinical correlations are found in the literature. A few factors that contributed to the discrepancies are methodological differences in the detection of antigens, size of the population studied, patients from one or multiple institutions, as well as factors such as age, cytogenetics and a number of different treatment protocols. Our results may contribute to more specific investigations of CD56 expression in AML at diagnosis, and they could help an assessment of prognostic value in a larger cohort submitted to a single treatment protocol. If the hypotheses of early mortality, lower CR rate, an equally early relapse and/or extramedullary invasion are confirmed in AML cases with CD56 expression, this data would be relevant to stratify patients, based on this risk factor. A possible use for the detection of this molecule in blasts through flow cytometry would be as a marker to assess MRD, as normal blasts do not express myeloid markers concurrently with CD56. Our data demonstrated that CD56 expression in the blasts of AML patients is indicative of shorter OS, therefore confirming published findings. The power of this study may be increased with the inclusion of a larger number of individuals. 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