The administration of TGF-β1 into the brain reduced infarct size in experimental models of ischemia [16]–[18], while antagonizing the endogenous actions of TGF-β1 with an injection of a soluble TGF-β type II receptor, which binds TGF-β1 and prevents its biological actions, resulted in a dramatic increase in infarct area [19]. This evidence concerns the gene TGFB1 and ischemia.