To address this question, we employed a B10.BR→B6 GVHD model and employed IL-34–/– (B6 background) mice as recipients, since the maintenance of microglial cell homeostasis is dependent upon interactions between the endogenous ligands CSF-1 and IL-34 with their cognate receptor CSF-1R (38, 39), and the genetic absence of IL-34 results in a significant reduction in microglial cell numbers (40). The gene discussed is CSF1R; the disease is graft versus host disease.