The developmentally regulated neuronal pathfinding and fasciculation defects we reported previously in Scn1b−/− cerebellum and corticospinal tract, coupled with the region‐specific cortical pyramidal neuron hyperexcitability observed in this study may contribute to the increased severity of SCN1B‐linked early infantile DEE in terms of seizure onset, seizure severity, or severity of co‐morbidities, including profound motor and cognitive delays, intellectual disability, autism spectrum disorders, and hearing loss in patients. The gene discussed is SCN1B; the disease is Intellectual disability.