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 SCN1A; the disease is Dravet syndrome.