Our data showing that Scn1b deletion impairs the excitability of PV + interneurons and alters the excitability of pyramidal neurons suggest that Scn1b‐linked early infantile DEE pathogenesis and Scn1a‐linked DS and VGSC GOF pathogenesis may share common elements. The gene discussed is SCN1B; the disease is developmental and epileptic encephalopathy.