The current data demonstrated that the alternative pathway proteins of the complement system were primarily overexpressed in PCOS, with increased C3, properdin and factor B; however, this appeared to be balanced by an increase in the inhibitory factors of this pathway, CFHR5, factor H and factor I, suggesting an inefficient complement activation system in the normal fasting condition in PCOS; however, the findings could be accounted for in part by BMI, hyperandrogenemia and insulin resistance. The gene discussed is C3; the disease is polycystic ovary syndrome.