Notably, this neonatal isoform has a more positive voltage-dependence of activation than the adult one, which may contribute to the relative hypoexcitability of the neonatal brain; moreover, since the effect of the mutation was specific for this neonatal variant, it appears likely that seizure disappearance after the neonatal period in BFNIS patients carrying this mutation is due to the switch between the two Nav1.2 isoforms or to the developmental switch between Nav1.2 and Nav1.6 channels (Liao et al., 2010b). The gene discussed is SCN2A; the disease is Benign familial neonatal-infantile seizures.