In keeping with our goal to pursue the development of G-CSF as a therapeutic agent to expand the limited therapeutic time window of tPA for ischemic stroke treatment, we conducted a follow-up study to examine whether the drug can reduce delayed tPA treatment-induced HT, worsening of neurological outcomes, and mortality in a thromboembolic (TE) model of stroke, a stringent model that closely mimics the clinical situation of vascular occlusion and reperfusion [14,15,16,17]. This evidence concerns the gene CSF3 and Stroke.