Another study achieved upregulation of SCN1A in inhibitory interneurons using an AAV to express a GABArgic cell-selective transcription factor, resulting to an increase in Nav1.1 protein expression.6 Additional safety studies in nonhuman primates (NHPs) showed good uptake of the construct throughout the brain and with no adverse events.6 In principle, these approaches can be used to upregulate any gene, and thus treat a range of LoF mutations causing epilepsy, although implementation requires substantial bioinformatic insights into promoter and enhance function. The gene discussed is SCN1A; the disease is epilepsy.