We focus on the PV + and SOM + subtypes of interneurons, based on recent findings that they change in number in human surgical samples.12 In the CD model, SOM + interneurons were lost in the DG hilus, similar to previous observations in experimental and human temporal lobe epilepsy.35,36 The early decrease may suggest developmental defects of SOM + interneurons in CD, including impaired migration, differentiation or reduced proliferation.37 The remaining SOM + interneurons were hyperactive, and changes in SOM activity correlated with seizure severity. Here, GRHL3 is linked to temporal lobe epilepsy.