Etiology of MOSH may be multifactorial and includes not only the diminished SHBG concentrations seen in obesity but also an increased aromatase activity, as well as the production of adipocytokines and gut derived endotoxins that impair kisspeptin signaling in the hypothalamus (and, consequently, GnRH secretion) [9,26]. The gene discussed is CYP19A1; the disease is obesity due to melanocortin 4 receptor deficiency.