This mechanistic relationship is also supported by clinical findings that showed differential changes in placental concentrations of total and phosphorylated Akt, AMPKα, and mTOR in women with normal pregnancies compared to those with pregnancies complicated by foetal growth restriction (FGR) or gestational diabetes (GDM) with children large-for-gestational-age (LGA) [52]. The gene discussed is AKT1; the disease is gestational diabetes.