Given the high expression levels of TLR8 in PV-interneurons and the fact that robust activation of TLR8 in neurons can induce neuronal death [17], it is tempting to speculate that non-canonical TLR8-signaling in hippocampal PV-interneurons may contribute to their degeneration in human epilepsy and in animal epilepsy models based on an initial status epilepticus or traumatic brain injury. Here, TLR8 is linked to status epilepticus.