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Twenty\u2010five percent of patients have imatinib resistance and treatment difficulties due to heterogeneity after progression, but little is known about the mechanism. A key transcription factor in hematopoiesis, MYB<\/jats:italic>, has been reported to increase abnormally in several types of aggressive blood disorders including CML.<\/jats:p><\/jats:sec>Methods<\/jats:title>This study used a zebrafish model to explore the relationship between BCR\/ABL1<\/jats:italic> and c\u2010myb<\/jats:italic> in CML progression. A CML zebrafish model was crossed with a c\u2010myb<\/jats:italic> hyperactivity transgenic line.<\/jats:p><\/jats:sec>Results<\/jats:title>It was found that both exogenous BCR\/ABL1<\/jats:italic> and c\u2010myb<\/jats:italic> could up\u2010regulate the expression of neutrophil\u2010related genes. More seriously, neutrophil accumulation was observed when BCR\/ABL1<\/jats:italic> was combined with c\u2010myb<\/jats:italic> overexpression. Further studies showed that c\u2010myb<\/jats:italic> may be one of the downstream targets of BCR\/ABL1<\/jats:italic> and the effect of BCR\/ABL1<\/jats:italic> on neutrophils was c\u2010myb<\/jats:italic> dependent. Taking advantage of this inheritable in vivo model, it was shown that a combination of imatinib and flavopiridol, a cyclin\u2010dependent kinase inhibitor targeting MYB<\/jats:italic>, could more effectively alleviate the aggressive phenotype of the double transgene line.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>In summary, this study suggests that c\u2010myb<\/jats:italic> acts downstream of BCR\/ABL1<\/jats:italic> and is involved in CML progression and is therefore a risk factor and a valuable target for the treatment of CML progression. The model used in the study could be helpful in high\u2010throughput drug screening in CML transformation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ame2.12282","type":"journal-article","created":{"date-parts":[[2022,10,27]],"date-time":"2022-10-27T10:20:45Z","timestamp":1666866045000},"page":"136-144","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["c\u2010myb<\/i> is involved in CML<\/scp> progression and is a therapeutic target in the zebrafish CML<\/scp> model"],"prefix":"10.1002","volume":"7","author":[{"given":"Yin","family":"Ye","sequence":"first","affiliation":[{"name":"Division of Cell, Developmental and Integrative Biology, School of Medicine South China University of Technology Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaojun","family":"Yang","sequence":"additional","affiliation":[{"name":"Division of Cell, Developmental and Integrative Biology, School of Medicine 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