In pregnancies complicated by GDM and/or maternal overweight or obesity, fetoplacental endothelial dysfunction appears to arise from dysfunction in the regulation of several critical pathways, including epigenetic modifications, inflammatory signalling, nitric oxide-mediated vascular signalling, mitochondrial function, and alterations in the L-arginine/nitric oxide and insulin/adenosine signalling axes (36, 37). The gene discussed is INS; the disease is gestational diabetes.