A single administration of T3 24 h after transient middle cerebral artery occlusion in rats increased the expression of brain-derived neurotrophic factor, nestin, and SRY-box transcription factor 2 [1], and the administration of T3 in the acute phase of ischemia in the experiment led to a decrease in the expression of aquaporin-4, a water channel protein that is involved in the formation of cerebral edema after ischemic stroke [1]. Here, AQP4 is linked to ischemic stroke.