The objectives of this review are (1) survey the evidence of the vital roles played by FoxP3+CD25+CD4+ Tregs in stroke pathophysiology, (2) discuss further investigations to fully elucidate the precise regulatory mechanisms of FoxP3+CD25+CD4+ Tregs in stroke, and (3) evaluate the possible therapeutic application and potential pitfalls of modulating the activity and quantity of FoxP3+CD25+CD4+ Tregs in stroke treatment. The gene discussed is FOXP3; the disease is Stroke.