The Espinosa group have investigated the underlying deficits in children with DS, in particular, those arising directly from the triplication of several immune-related genes on the q arm of Hsa21, including four of the six interferon receptors (IFNAR1, IFNAR2, IFNGR2, and IL10RB) and several interferon-related signalling proteins operating within the innate immune system (MX1, MX2, CCT8)11 and these too are worthy of future studies in our DS cohorts. The gene discussed is CCT8; the disease is Dravet syndrome.