The mode of action (and target) unique to epilepsy-inducing effects involved nuclear receptor agonists (retinoid receptor and constitutive androstane receptor), metabolic control inhibitors (thyroid peroxidase, antifolate, dehydrogenase, and carbonic anhydrase), processes involving inhibition of immunomodulation (atherogenesis and cytokine production), and inhibition of signal transduction (PKC and PKA). This evidence concerns the gene PRRT2 and epilepsy.