In animal stroke models, depletion of TGF-β1 has been shown to increase inflammatory responses and deteriorate microglial CNS homeostatic function [55], whereas delivery of TGF-β1 protein via intravascular or intranasal delivery routes attenuated poststroke neuroinflammation and improved the functional outcome [20, 49, 56–58]. The gene discussed is TGFB1; the disease is stroke disorder.