In summary, we showed that activated Tregs promoted NSC proliferation in ipsilateral SVZ of normal and ischemic mouse brains and blocking IL-10 abolished activated Tregs-mediated NSC proliferation, suggesting that the activated Treg/IL-10 pathway plays a critical role in neurogenesis in the SVZ after focal ischemia which may provide a new therapeutic approach for ischemic stroke. The gene discussed is IL10; the disease is ischemic stroke.