Taking these results together, we speculate that the HMGB1 released from different sources in response to epileptogenic stimuli may mediate the specific processes leading to status epilepticus, with increased neuronal excitability, including glutamate release, upregulation of IL-1b, TNF-a, TLR-4, and disruption of the BBB [21,25,111,112]. This evidence concerns the gene TLR4 and status epilepticus.