In silico model reveals the key role of GABA in KCNT1-epilepsy in infancy with migrating focal seizures.

This study illustrates the interest of biomathematical models to explore pathophysiological mechanisms bridging the gap between the functional effect of gene pathogenic variants and specific EEG phenotype. Such models can be complementary to in vitro cellular and animal models. This multiscale approach provides an in silico framework that can be further used to identify candidate innovative therapies.