In this study, Foxo1&4 were DE in Lin-/VEGF-R2+ D-EPCs, which may contribute to Lin-/VEGF-R2+ D-EPCs dysfunction observed through a negative effect of hyperglycemia-induced oxidative stress on the regulatory interaction between Pik3c2a/Foxo1 and the possible activation of the P66shc-Akt-Foxo pathway. This evidence concerns the gene AKT1 and Hyperglycemia.