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Our current investigation in a mouse CML model revealed dominant presence of neutrophils during CML progression, accompanied by significant reductions and exhaustion of T cells. In coculture, these BCR\u2013ABL1 expressing neutrophil\u2010like CML cells significantly inhibited T cell proliferation. Gene expression profiling revealed that there was a global activation of both neutrophil markers and related immune suppression genes in these CML cells. Correlative analysis revealed strong correlations between the expression of BCR\u2013ABL1 and immune suppression genes, suggesting a potential regulation of those genes by BCR\u2013ABL1. Importantly, we identified CEBPB as a critical transcription factor that directly regulated the expression of master immune modulators TGFB1 and ARG2 through promoter binding, in both human and mouse CML samples. Therefore, blocking BCR\u2013ABL1, or its downstream C\/EBP\u03b2, TGF\u2010\u03b2 and arginase with inhibitors or shRNAs\u00a0rescued T cell suppression by neutrophil\u2010like CML cells. 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