In contrast to these animal models of transient ischemia contributing to the specific hippocampal neuronal death, in another animal model (permanent cerebral infarction using middle cerebral artery occlusion in rats), there was persistent up-regulated expression of Gal-3 in the ischemic lesions at day 1 after occlusion; the number of Gal-3 positive cells in the cerebral infarction was further increased on days 2 and 3, and peaked at day 7 after occlusion [85]. The gene discussed is LGALS3; the disease is cerebral infarction.