Proinflammatory cytokines (IL-1β, IL-6, and IL-18) contribute to the pathophysiology of epilepsy through several pathways: modulating glutamatergic transmission [32], enhancing N-methyl-D-aspartate receptor function by activation of SRC tyrosine kinase [33], and altering GABAergic neurotransmission [34]. Here, IL1B is linked to epilepsy.