The findings of studies conducted by us and others indicated that pharmacological inhibition of the subunits of sulfonylurea receptor 1-transient receptor potential M4 (SUR1-TRPM4) or gene deletion of Trpm4 could function in preserving BBB integrity in animal models of status epilepticus [13], acute ischemic stroke [14], spinal cord injury [15], intracerebral hemorrhage [16], and subarachnoid hemorrhage [17]. This evidence concerns the gene TRPM4 and status epilepticus.