TGF-β1 administered into the brain reduced the infarct size in experimental models of ischemia [24]–[26] while antagonizing the endogenous action of TGF-β1 with the 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 [27]. Here, TGFB1 is linked to ischemia.