What is interesting to note is that based on these findings, the production of IFN-γ may contribute to the production of excess androgen in PCOS; by stimulating granulosa cell apoptosis, IFN-γ eliminates the aromatase enzyme in these cells and therefore ensures that the steroid synthesis pathway ends at androgen rather than estrogen. This evidence concerns the gene CYP19A1 and polycystic ovary syndrome.