Their data support the idea that non-F4/80 cells (ie, F4/80-Ly6G+ granulocytes) may play a role in a separate subset of island function, particularly as related to myelopoiesis following anemia of inflammation, leading to a dynamic antagonistic balance between granulopoiesis and erythropoiesis, a notion supported by the dramatic effects of G-CSF treatment on suppression of erythropoiesis (Jacobsen et al., 2014; Jacobsen et al., 2015). The gene discussed is CSF3; the disease is anemia.