Moreover, when we used AKT agonists and inhibitors to treat cells separately, we found that phosphorylated FoxO1 was enhanced or weakened with the enhancement or decrease of phosphorylated AKT, respectively, no matter how ITGA2 changed, which indicates that ITGA2 regulated the biological behavior of ovarian cancer cells by acting on the AKT/FOXO1 axis. This evidence concerns the gene AKT1 and ovarian carcinoma.