SCN1A and Dravet syndrome: In an attempt to circumvent the size obstacle, strategies for DS therapy have included (i) enhanced expression of the endogenous Scn1a via transcriptional activation (5–8); (ii) overexpression of SCN1B, which encodes NaVβ1, an auxiliary subunit that increases NaV1.1 channel complex efficacy (9); and, (iii) antisense oligonucleotide–mediated downregulation of SCN8A (10).