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Figure 5: Roles of hnRNPs in the impaired granulocytic differentiation of BCR/ABL transformed myeloid progenitor cells. Both hnRNP E2 and FUS function as the downstream regulators of BCR/ABL oncoprotein and have been implicated in chronic myelogenous leukemia by preventing granulocytic differentiation from myeloid progenitor cells through inhibiting G-CSFR and blocking G-CSF signaling, which finally disrupt the normal myeloid cell differentiation or maturation pathway, resulting in myeloid progenitor cell accumulation abnormally in the bone marrow and circulation.