By recognizing the imbalance of these two GR isoforms in the dysplastic brain region compared to an adjacent relatively non-dysplastic region, which could be a biomarker of the dysplastic focus, and the effect of GRβ on drug response in BBB endothelial cells, the mechanism underlying the BBB involvement in drug-resistant epilepsy is further unveiled. This evidence concerns the gene NR3C1 and epilepsy.