Spratt et al. (2021) observed a similar reduction in AP amplitude in an Scn2a knockout mouse model, and correspondingly explained neocortical pyramidal cell hyperexcitability by attenuated hyperpolarizing potassium currents. Thus, reduced potassium currents might explain excitatory neuronal hyperexcitability, as a secondary effect to SCN1A deficiency in DS. This evidence concerns the gene SCN2A and Dravet syndrome.