Non‐convulsive absence seizures have been observed in heterozygous SCN8A/NaV1.6 knock‐out mice, and floxed models with selective knock‐out in selective neurons have shown that they are generated by reduced desynchronizing recurrent synaptic inhibition in neurons of the thalamic reticular nucleus leading to prolonged synchronized inhibitory output affecting the timing of thalamocortical oscillations and to spikes and wave discharges (absence‐like phenotype) (Makinson et al., 2017). The gene discussed is SCN8A; the disease is juvenile absence epilepsy.