Specifically, we believe that the vasogenic edema in PRES was reduced with mannitol treatment, which increased the hyperosmotic stress and opened the blood–brain barrier; meanwhile, upregulation of aquaporin-4 expression secondary to the increased osmotic pressure resulted in cytotoxic edema in the astrocytes in SCC (RESLES). The gene discussed is AQP4; the disease is Posterior Leukoencephalopathy Syndrome.