It has been further conjectured that comorbid depression may commonly confound CFS studies [36] and, just as this may lead to erroneous finding of increased rates of childhood adversity in CFS, similarly, it may explain the methylation pattern [66] including in the NR3C1-1F promoter region [33], the increased GR function (shown using the DST, the dex/CRH test [28], or ex vivo measures), and the basal hypocortisolaemia which have been (inconsistently [10]) shown in previous CFS studies. This evidence concerns the gene NR3C1 and depressive symptom measurement.