At the ovarian level, excess androgens suppress granulosa cell proliferation through mechanisms such as upregulating phosphatase and tensin homolog (PTEN) expression, which is PPARγ-dependent, or by disrupting WNT signaling, both of which lead to follicular arrest and polycystic ovary formation (Chen et al., 2015; McFee et al., 2021). The gene discussed is PTEN; the disease is polycystic ovary syndrome.