It has been demonstrated in tests carried out on human umbilical vein endothelial cells (HUVEC) cells, obtained from pregnancies with GDM, that both high glucose and GDM induce endothelial dysfunction through a mechanism mediated by an increase in the expression of miRNA-101 and a reduced expression of histone methyl transferase enhancer of zester homolog-2 (EZH2-ß), which reduces trimethylation of lysine 27 in Histone 3 [117]. Here, EZH2 is linked to endothelial dysfunction.