Regarding the involvement of inflammation and oxidative stress in the pathomechanism of epilepsy, it was suggested that targeting molecular signaling pathways, such as the IL-1β-IL-1 receptor type 1 and TLR4, P2X7 receptors and transcriptional antioxidant factor Nrf2, did not prevent epilepsy development but might have clinically relevant disease-modifying effects [41]. Here, TLR4 is linked to epilepsy.