Nevertheless, since the vasculature is also a source of cells that contribute to scar formation in the lesioned area [35], which could, therefore, impede structural and functional recuperation after stroke, other processes alongside the above-mentioned neovascularization could also contribute to the G-CSF-induced improvements in neurological and behavioral functions in stroke rats subjected to delayed tPA treatment [6,7,8,9,10,11,12]. The gene discussed is CSF3; the disease is stroke disorder.