AKT1 and gestational diabetes: In this phenomenon insulin would be acting as a factor that restores a potential GDM-associated metabolic phenotype (i.e., preferential activation of p42/44mapk over Akt pathways) to a normal, mitogenic phenotype (i.e., preferential activation of Akt over p42/44mapk pathways) by restoring IR-A expression to values in HUVEC from normal pregnancies [7].