Despite clear evidence of severe epilepsy, broad neurologic dysfunction, and early death in the Scn1a deficient mouse model used here (Miller et al., 2014; Mistry et al., 2014; Tran et al., 2020), we found only subtle changes to synaptic inhibition, and overall, synaptic integration and input/output functions were relatively unchanged in the hippocampus of this DS model. The gene discussed is SCN1A; the disease is Dravet syndrome.