G-CSF is the key hematopoietic cytokine involved in the control of neutrophil development; therefore, it is a critical regulator of innate immunity against bacterial infections. G-CSF mobilizes stem cells indirectly by downregulating the expression of CXCL12 on marrow osteoblasts and by releasing neutrophil and monocyte proteolytic enzymes, including neutrophil elastase, cathepsin G, and matrix metalloproteinase-9. This in turn degrades important HSC-trafficking and adhesion molecules, such as c-kit, VCAM-1, and CXCR4. 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 also in 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.