This lack of selectivity likely limits the benefits of sodium channel inhibitors since LoF variants of NaV1.1 are known toimpair inhibitory interneuron function and causegeneralized epilepsy with seizures plus (GEFS+) and SCN1A-DEE (Dravet Syndrome) (Catterall et al., 2010; Claes et al., 2001; Escayg et al., 2000; Gennaro et al., 2003).Thus, inhibiting NaV1.1 may counter the benefit of inhibiting the sodium channels of excitatory neurons. The gene discussed is SCN1A; the disease is epilepsy.