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Background Previous studies identified KLF2 as a key "molecular switch" that regulated the expression of TF, and eNOS.And we built on these initial observations and provided evidence that rapamycin induced the expression of KLF2in human umbilical vein endothelial cells (HUVECs).PI (3, 4, 5) P3 mediates activation of protein kinase B, which phosphorylates and inactivates Foxos, thereby terminating expression of KLF2 and its target genes.We hypothesized that rapamycin might induce the expression and activity of KLF2 through nonphosphorylates and activates Foxos.