Dysfunctional NaV1.2 channel activity due to mutations in SCN2A has been linked to a range of neurological disorders, including infantile epileptic encephalopathy, benign (familial) infantile seizures, and autism spectrum disorder/intellectual disability.[10a] Specifically, gain‐of‐function (GOF) mutations of SCN2A are strongly associated with the development of epilepsy,[10, 11] as they result in enhanced NaV1.2 channel activity, leading to a hyperexcitable state in neurons and increasing the onset frequency of seizures. Here, SCN2A is linked to genetic developmental and epileptic encephalopathy.