The development of cytotoxic edema reportedly involves aberrant regulation of ion transport channels expressed on vascular endothelial cells (e.g., Na-K-Cl cotransporter 1 (NKCC1), which plays a role in the brain edema associated with ischemic stroke) and the sulfonylurea receptor 1–transient receptor potential cation channel subfamily M member 4 (SUR1-TRPM4) (39). Here, TRPM4 is linked to ischemic stroke.