G-CSF is the key hematopoietic cytokine involved in the control of neutrophil production and therefore is a critical regulator of the innate immunity against bacterial infections. G-CSF mobilizes stem cells indirectly by down-regulating the expression of CXCL12 on marrow osteoblasts and by releasing neutrophils and monocyte proteolytic enzymes, which include neutrophil elastase, cathepsin G, and MMP9. In turn, they degrade important HSC-trafficking and adhesion molecules including c-kit, CXCR4, VCAM-1(CD106), fibronectin, and OPN, which leads to reduced cellular adhesion of HSC through their receptor VLA-4 to bone marrow stroma. In addition, G-CSF possesses immunosuppressive effects on monocytes/ macrophages, dendritic cells, and T lymphocytes. The receptor for G-CSF is expressed not only in hematopoietic cells, but is also expressed on cardiomyocytes, skeletal muscle, and neurons. G-CSF influences mouse skeletal muscle development and regeneration by stimulating myoblast proliferation. In vitro, G-CSF displays strong antiapoptotic activity in neuronal cells. The beneficial effects of G-CSF have been demonstrated in rodent stroke models. G-CSF is used in patients with leukocytopenia and in donors of peripheral blood-derived hematopoietic progenitor cells prior to collection for transplantation.