These findings, together with triplication of the βAPP gene in DS and experimental evidence of neuronal stress-induced increases in βAPP expression and parallel secretion of sAPP for resultant activation of microglia, evidenced by increases in oxidative markers and overexpression and release of IL-1β, suggest that triplication of chromosome 21 genes, perhaps especially βAPP, may account for most of the very early neuroinflammatory and oxidative changes in DS. This evidence concerns the gene IL1B and Dravet syndrome.