At present, we treat patients with many genetic causes of DEE in infancy, including genes encoding sodium or potassium channel subunits, tuberous sclerosis, and congenital metabolic diseases.[50] In addition, Nappi et al revealed that mutations in KCNQ2, KCNQ3, and more rare KCNQ5 genes are related to DEE and described the clinical characteristics and pathogenesis of DEE patients with new KCNQ5 variants.[39]. Here, KCNA3 is linked to developmental and epileptic encephalopathy.