SCN1A and epilepsy: Additionally, recent discoveries of mutations in epilepsy syndromes in ion channels that would be expected to promote increased inhibition, such as SCN1A and potassium channel gain of function mutations, along with upregulation of inhibition in models of absence epilepsy, suggest that E/I imbalance as a general predisposing factor for epilepsy may not be a sufficient descriptor of the condition itself (Miri et al., 2018; Shao et al., 2019; Owen et al., 2021).