In a mouse model of Dravet syndrome with a hemizygous gene deletion (i.e., Scn1a +/-), it was observed that fast-spiking PV interneurons cells could no longer fire at their characteristically high frequencies (Fig 4C), with a smaller but significant effect also observed in Sst-expressing Martinotti cells [5]. The gene discussed is SST; the disease is encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.