In the hippocampus, for example, a reduction in the amount of SOM is considered a marker of epilepsy, but the mRNA levels increase for SOM interneurons in the kainic acid (KA) model of temporal lobe epilepsy, suggesting that the seizures may trigger SOM expression, and their receptors may be targets for anticonvulsive drug therapy [18]. Here, GRHL3 is linked to temporal lobe epilepsy.