In the kainate model of epilepsy, only intranasal treatment with Lnn, unlike other PUFAs, resulted in the suppression of cell death in the CA1 and CA3 regions of the hippocampus [23] through the activation of NF-κB [24,25], which, in addition to activation of the inflammatory response, is involved in the mechanism of neuroplasticity. Here, NFKB1 is linked to epilepsy.