Treatment with G-CSF causes mobilization of HSCs/HPCs and triggers fever. By acting on catecholaminergic cells (nerve cells or other), G-CSF increases the adrenergic tone in the marrow, thereby generating catecholamines that in turn activate neutrophils through the β3-adrenergic receptor (β3R; inset). As a consequence of adrenergic stimulation, neutrophils produce PGE₂, which can target osteoblastic cells through the EP4 receptor to promote HSC/HPC retention. Additionally, neutrophil-derived PGE₂ causes fever by systemically acting on the brain. Professional illustration by Somersault18:24.