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473 serial FISH testing at diagnosis and relapse. Cy‐ togenetic evolution was defined as the acquisition or loss of a cytogenetic abnormality at the sec‐ ond FISH testing and was observed in 14 patients (48%). Chromosome 17p deletion was identified as the most common acquired feature, found in 7 out of 29 patients (24%), with an established FISH cutoff of 7%. The presence of cytogenetic evolu‐ tion had a negative impact on PFS, with a median PFS of 3.9 months in patients with cytogenetic evolution versus 9.3 months in those with stable cytogenetics. Univariate and multivariate analy‐ ses identified del(17p) as a predictor of shorter PFS and OS. Patients who acquired del(17p) dur‐ ing the course of the disease achieved a signifi‐ cantly shorter PFS of 1.5 months compared with those who did not acquire del(17p) and achieved PFS of 8.9 months. In univariate analysis, stable cytogenetics predicted longer OS of 3.8 years, whereas patients with cytogenetic evolution had an OS of 3.1 years. Some of the limitations of the study by Salomon ‐Perzyński et al1 were acknowledged by the authors and include the retrospective design of the study, the limited number of participants, and the fact that the patients were not treated uniformly, having little access to novel antimy‐ eloma drugs. Another caveat is the fact that the authors did not separately evaluate the occurrence of cytoge‐ netic evolution in the patients tested at the first clinical or biochemical relapse as compared with the ones tested at subsequent clinical relapses. It is a well ‐known fact that MM evolution is char‐ acterized by progressive aggressiveness and lack of response to therapy as the disease unfolds. The authors stated that the refractory status to proteasome inhibitors (PIs) and / or immuno‐ modulatory drugs (IMiDs) and refractoriness to the last treatment line before the second FISH The complex genetic heterogeneity, expressed at both interpatient and individual levels, is the driving force behind the natural evolution and the treatment response in multiple myelo‐ ma (MM). Large ‐scale studies have demonstrated that certain cytogenetic mutations, such as chro‐ mosome 17p deletion (del[17p]), t(4;14), t(14;16), or 1q gain, noted at the time of diagnosis rep‐ resent high ‐risk cytogenetic features and are correlated with a worse prognosis in terms of progression ‐free survival (PFS) and overall sur‐ vival (OS). Although acquired structural changes are a common feature at relapse, little is known about the impact of the genetic evolution on the treatment response and progression of MM. The emergence of genetically altered clones is the result of Darwinian evolution under the se‐ lective pressure exerted by treatment. Chro‐ mosome 17p deletion is considered a high ‐risk feature in newly diagnosed MM and can be ob‐ served through fluorescence in situ hybridization (FISH) evaluation in 10% to 20% of patients, de‐ pending on the cutoff used. The loss of the short arm of chromosome 17 is correlated with TP53 tumor suppressor gene silencing. Usually, it is a secondary event in the evolution of MM, but the currently existing data are inconclusive as to whether the subsequent occurrence of del(17p) bears the same unfavorable impact as in newly diagnosed patients. In the current issue of Polish Archives of Internal Medicine (Pol Arch Intern Med), Salomon ‐Perzyński et al1 retrospectively analyzed the occurrence of cytogenetic evolution using an interphase FISH test for t(4;14), t(14;16), and del(17p) on magneti‐ cally selected CD138 ‐positive plasma cells. Among the 650 patients evaluated in the Warsaw Depart‐ ment of Hematology between 2014 and 2019, the authors selected 177 who had a complete set of data. Out of these, 29 patients with MM had EDITORIAL