WBCs recovered from CML patients contained only small amounts of the 24 kDa isoform of FGF-2, although the level of soluble FGF-2 in plasma was significantly increased. While searching for the potential source of FGF-2 in the blood of these patients, with exclusion of the possibility of a concomitant occurrence of solid tumors and noncancer diseases. Nevertheless, other possible sources of FGF-2 in plasma of CML patients should be considered. One of them is the rapidly proliferating blasts that are present in bone marrow, while being rare in peripheral blood. During progression of CML, especially in its terminal stages, large numbers of proto-differentiated blasts are released into the bloodstream. FGF2 expression was increased in CML and AML stroma during the development of resistance to kinase inhibitors, indicating that FGF2 expression is a regulated autocrine growth factor for stroma. In stress hematopoiesis (highly complex and dynamic process that involves crosstalk between HSPCs, bone marrow stromal cells, and nonhematopoietic tissues to sense apathogenic organism and convert the signal of an infection into the signal for myeloid differentiation), FGF2 stimulates expansion of both supportive marrow stromal cells and hematopoietic stem/progenitor cells to regenerate the marrow. There is evidence that stress hematopoiesis is a frequent event in CML, because up to 35% of CML patients treated with Imatinib (IM) and newer agents develop transient cytopenias.