The intricate connection between SST+ interneurons and seizures goes beyond a simple association, exemplified by a decrease in SST+ interneuron activity in the neocortex observed in Dravet syndrome, an example of a monogenic epilepsy caused by a pathogenic variant in the SCN1A gene [57]. This evidence concerns the gene SST and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.