A comparison of cell-free RNA levels from the amniotic fluid surrounding TS or euploid female foetuses, which circumvents some of the aforementioned problems, has hinted at dysregulation of the hematologic/immune system in TS and has highlighted a number of specific X-linked and autosomal candidate genes for TS phenotypes [73]; of these, three have previously been tentatively linked to idiopathic ADHD by genetic association studies (FEN1/ELOVL6 [74], GSK3B [75] and BAIAP2 [76]) and as such may be regarded as potential modulators of ADHD risk both within TS and within the general population. The gene discussed is GSK3B; the disease is attention deficit-hyperactivity disorder.