Since GDM associates with overexpression of insulin receptor A (IR-A) form in HUVECs, and activation of these receptors leads to preferential p42/44mapk phosphorylation compared with Akt phosphorylation in HUVECs from normal pregnancies, it is feasible that insulin mediates similar mechanisms to restore p42/44mapk associated cell signalling in a high D-glucose environment and in GDM. The gene discussed is AKT1; the disease is gestational diabetes.