Abstract: Objective To investigate the expression of PI3K/AKT/GSK3 signal pathways of endometrial lesions in Polycystic Ovary Syndrome (PCOS) patients with insulin resistance and non-insulin resistance and to determine the mechanism of insulin in endometrial lesions in PCOS patients. Methods 34 cases of PCOS patients as treatment group and 30 cases of patients with sterility due to oviduct diseases and treated through uterus curettage as control group were selected and involved in this study. The OGTT, INS experiment and 6 items of sex glands were determined in patients of treatment group, and divided PCOS patients in to groupⅠ (insulin resistance group) and groupⅡ (Non-insulin resistance group) depending on whether existed insulin resistance. The expression of PI3K (phosphatidylinositol 3-kinase), p-AKT (PPKB, phosphorylated protein kinase B) and GSK3 (glycogen synthase kinase 3) in paraffin section specimen of endometrial were determined by immunohistochemical methods. Results The express level of PI3K in PCOS patients were higher than that in control group (P<0.01) with the highest level in group I. The express level of p-AKT in PCOS patients were higher than that in control group (P<0.01) with the highest level in group I. There were no significant difference among the express level of GSK3 in group I, groupie and control group (P>0.05). Conclusion Insulin signal pathways PI3K and p-AKT may be the signal transduction pathways of endometrial lesions in PCOS patients with insulin resistance.