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Granulocyte production increases following infection or in response to cytokine stimulation, and activation of the <jats:styled-content style=\"fixed-case\">CCAAT<\/jats:styled-content>\/enhancer\u2010binding protein \u03b2 (C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2) transcription factor is required for such stress\u2010induced granulopoiesis, whereas C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b1 plays a critical role in maintaining steady\u2010state granulopoiesis. Different roles of these C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content> transcription factors in different modes of hematopoiesis are evolutionally conserved from zebrafish to humans. In addition to reactions against infections, C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 is responsible for cancer\u2010driven myelopoiesis, which promotes cancer progression, at least in part, by abrogating the immune response in the cancer microenvironment. The <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">ABL<\/jats:styled-content> fusion protein activates emergency\u2010specific pathway of granulopoiesis by upregulating C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2. This in turn causes chronic phase chronic myeloid leukemia, which is characterized by myeloid expansion. The C\/<jats:styled-content style=\"fixed-case\">EBP<\/jats:styled-content>\u03b2 transcription factor also plays a role in other hematological malignancies of both myeloid and lymphoid lineage origin. 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