The approaches that aim to increase the sodium voltage‐gated channel alpha subunit 1 protein (Nav1.1) in patients with Dravet syndrome and that have entered clinical studies comprise a viral vector–based therapy with expression of a transcription factor as well as an antisense oligonucleotide‐based approach targeting an alternate splicing event (https://clinicaltrials.gov/study/NCT04740476).7, 8. This evidence concerns the gene SCN1A and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.