In addition, we demonstrated for the first time that CA suppressed neuroinflammation by inhibiting the biological function of ACOD1 and ACOD1-mediated activation of PERK-NF-κB inflammation signaling pathway, suggesting that the inhibition of ACOD1 enzymatic activity could be regarded as a therapeutic strategy for neuroinflammatory associated disorders including epilepsy. Here, NFKB1 is linked to epilepsy.