That low SHBG levels are often associated with fatty liver disease and hyperinsulineamia in adolescents with mild PCOS may reflect a novel hepato-ovarian axis [96]: reduction of hepatic SHBG synthesis in NAFLD causes increased androgen bioavailability as the initial stage of PCOS, but persistent increases in free androgen in the blood stream eventually causes ovarian dysfunction with excess secretion of androgens (hyperandrogenism). This evidence concerns the gene SHBG and hyperandrogenism.