Given the fact that insulin+hCG-treated rats exhibit peripheral insulin resistance (Fig. 1), hyperandrogenism (Table 2), ovarian defects (Tables 1 and 2), and disrupted estrous cyclicity (Table 1 and Supplemental Table 2)22, 23, 24, 25, 26 in a similar manner as human PCOS, it is worth examining whether uterine dysfunction occurs in these rats in addition to both the metabolic and ovarian features of PCOS. The gene discussed is INS; the disease is polycystic ovary syndrome.