If indeed FSH-R3 (which lacks exon 10) is the key player to mediate FSH action on stem cells resulting in neo-oogenesis during postnatal life, one could easily explain why the extensive studies undertaken to search for mutations in the exon 10 of FSH receptor in cases of amenorrhea [39] and ovarian tumors [40] have failed to yield any results. This evidence concerns the gene FSHR and amenorrhea.