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 epilepsy.