While both treatments mimic ovarian disfunctions, hyperandrogenism, and oligo‐anovulation, the prenatal testosterone exposure also produces the metabolic imbalances typical of PCOS.[51] In sheep, prenatal exposure to androgens produces traits characteristic of PCOS with elevated frequency of LH pulses, hyperandrogenism and oligo‐anovulation.[52] In zebrafish, exposure of young females to testosterone also produces a PCOS model with follicular growth‐arrest, ovary enlargement, reduced ovulation rate, and a decrease in reproduction.[53]. This evidence concerns the gene PLOD1 and polycystic ovary syndrome.