When comparing de novo variants in patients with neurodevelopmental disorders, individuals with missense variants have been reported to be generally more likely to develop epilepsy than individuals with truncating variants, and enrichment was observed in genes associated with ion channel‐encoding genes (KCNQ2, SCN1A, and KCNH1),42, 43, 44 suggesting a dominant‐negative or gain‐of‐function effect of KCNH1 variant in the pathophysiology of epilepsy. This evidence concerns the gene SCN1A and epilepsy.