In our previous study [81], we have demonstrated neuronal protection by G-CSF protein in hypoxia–ischemia animal model was in part due to its anti-inflammatory action since the expression levels of pro-inflammatory cytokines, TNF-α and IL-1ß were significantly decreased in the G-CSF protein treated group, while the anti-inflammatory cytokine, IL-10, expression level was increased. The gene discussed is CSF3; the disease is ischemia.