GCK and Glucose intolerance: To explore whether reduced maternal Tet3 expression was the only contributor to Gck hypermethylation and glucose intolerance in offspring, they generated a Tet3 knockout mouse, in which Tet3 expression was insufficient due to oocytes‐specific Tet3 heterozygous and homozygous knockout, mimicked the effect of maternal hyperglycaemia.