Supporting the idea that high LH levels are responsible for the adrenocortical hyperactivity in nonobese PCOS women, Kero et al. [33] showed the development of polycystic ovaries and bilateral adrenal hyperplasia, with increased androgen and cortisol production, in a transgenic mouse model with a high constitutive LH production. This evidence concerns the gene PLOD1 and polycystic ovary syndrome.