While the exact pathogenesis of ADS is unknown, studies show that compared to individuals with JIA, those with ADS show an expansion of IgM memory B cells, decreased proportion of transitional B cells, increased TNF and INF-γ responses by CD8 T cells, increased TNF and IL-17A responses by CD8 T cells, significant expansion of Th1/Th17 cells, and reduced Treg cells, collectively suggesting immune dysregulation in individuals with DS [64, 67]. This evidence concerns the gene CD40LG and Dravet syndrome.