Further, this may explain why human pathologies caused by heterozygous mutations in COMPASS methyltransferases, such as Wiedemann–Steiner syndrome (caused by mutations in KMT2A) and subgroups of generalised dystonia (KMT2B) and Kabuki syndrome (KMT2D), do not present with glucose intolerance and hyperglycaemia; compensation by other methyltransferases means that it is unlikely that H3K4me3 is reduced to an extent that impairs beta cell function. This evidence concerns the gene KMT2A and Hyperglycemia.