Mutations in the sodium channel NaV1.1, encoded by SCN1A, are associated with a range of epileptic disorders in which febrile seizures with varying rates of severity are involved, such as Dravet syndrome (DS), generalised epilepsy with febrile seizures plus (GEFS+) and familial febrile seizures (FS). It is thought that NaV1.1 deficiency leads to a reduction in firing of GABAergic inhibitory interneurons which causes an imbalance between excitation and inhibition, resulting in a hyperactive network. Alternatively, a hyperactive network can also result from an increase in excitatory signalling, for example through increased excitatory GABA. Accordingly, a delay in the hyperpolarising GABA shift has been associated with a variety of neurodevelopmental disorders, including DS. Moreover, the genotype-phenotype relationship currently remains unclear, where the same SCN1A mutation can lead to different clinical phenotypes, even between family members. In this study, we aim to assess the maturation of the GABAergic system in SCN1A-related epilepsy using iPSC-derived neurons using immunocytochemistry and MEA recordings. Preliminary results suggest a link between the timing of the GABA shift and the severity of the clinical phenotype, which we explore as a potential mechanism behind the development of different clinical phenotypes.