It is hypothesized that in the context of epilepsy, Due to its ability and propensity to attenuate Nav1.1 sodium current and resulting in reducing the excitability of inhibitory neurons, Nav1.1 mutations, regardless of being missense or nonsense, gain-of-function or loss-of-function, and their association with GEFS + or SMEI, all stem from it. This evidence concerns the gene SCN1A and epilepsy.