The emergency hematopoiesis represents a physiological response of the immune system to infections that is governed by (a) direct stimulation of progenitor cells via Toll-like receptors (TLRs) [5], (b) production of growth factors and cytokines by the bone marrow (BM) niche-forming cells and mature hematopoietic cells (like granulocyte colony-stimulating factor, or G-CSF) [6], and (c) paracrine effects of TLR-activated HSCs [7]. Here, CSF3 is linked to infection.