Insulin signaling is complicated, and any changes in the process, such as phosphorylation of insulin receptors, insulin receptor substrate-1, or the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) pathway and the subsequent expression of glucose transporter 4 (GLUT4), may play a role in the insulin-resistant state of PCOS [3]. This evidence concerns the gene AKT1 and polycystic ovary syndrome.