Here, Shao and colleagues used an established DS model (Scn1aRX/+ which results in NaV1.1 haploinsufficiency) combined with an elegant genetic strategy to either selectively ablate tau in excitatory or inhibitory neurons, or to obtain a ubiquitous TAU downregulation using antisense oligonucleotides.7 This evidence concerns the gene SCN1A and Dravet syndrome.