Molecular and cellular changes, such as variations in the expression of GFAP (indicative of astrocyte response), GAT1 (a GABA transporter affecting neurotransmitter uptake), and Kir4.1 (a potassium channel involved in glial buffering), pave new paths for therapeutic interventions in epilepsy, beyond merely neurochemical alterations involving neurotransmitters, by encompassing broader aspects like receptor activity, structural changes, and glial proliferation. The gene discussed is KCNJ10; the disease is epilepsy.