Our results seem to indicate that the wild-type genotype for SNV rs2298771 in SCN1A, which encodes the voltage-gated sodium channel—NaV1.1 sodium channel alpha subunit—results in a loss-of-function protein presenting a lower expression, with an insufficiency of NaV1.1, as observed in the SCN1A gene mutated in Dravet Syndrome, as well as milder phenotypes associated with genetic epilepsy with febrile seizures plus [34,36,37]. The gene discussed is SCN1A; the disease is encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.