Non‐technical summary In some forms of incurable epilepsies, GABAergic interneurons, which physiologically mediate inhibition in the brain, are thought to mediate excitation. The presence of a specific form of electrical communication between these cells, which is mediated by structures called gap junctions, has been proposed to be involved in the generation of synchronized epileptiform discharges. In support of this hypothesis is the repeated finding in the literature that the drug carbenoxolone, which is an effective blocker of gap junction function, decreases epileptiform activity in models of epilepsy bothin vivoandin vitro. Our work challenges this view and highlights additional side‐effects of carbenoxolone, which are unrelated to gap junctions, but seem to contribute to its reported antiepileptic activity. A full knowledge of these additional mechanisms is important for the rational development of new molecules to be used in the therapy of epilepsy.