Nevertheless, the analyses of longitudinal samples collected from an individual undergoing periodic treatments with the JAK inhibitor tofacitinib demonstrated that IFN hyperactivity is attenuated in this individual without overt immune suppression, with consequent normalization of many transcriptional signatures dysregulated in DS, thus involving elevated JAK/STAT signaling as a driver of many of the changes observed. The gene discussed is SOAT1; the disease is Dravet syndrome.