In addition to causing autistic‐like phenotypes, heterozygosity for the Scn2a knockout allele (i.e., Scn2a+/–) also acts as a protective modifier of epilepsy and sudden death in mice carrying a deletion of the Kcna1 gene (i.e., Kcna1–/–), which encodes Kv1.1 voltage‐gated potassium channel α‐subunits that regulate axonal excitability (Mishra et al., 2017). This evidence concerns the gene KCNA1 and epilepsy.