Hippocampal-specific SCN1A deletion reduces the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) in dentate granule cells without altering excitatory inputs, directly leading to thermosensitive seizures and spatial memory deficits, which establishes inhibitory input deficiency in hippocampal microcircuits as a neurobiological basis for DS comorbidities (Stein et al., 2019). The gene discussed is SCN1A; the disease is Dravet syndrome.