In spite of unaltered cortisol levels in relation to MS found in their study, Foroughipour et al. [22] hypothesized that chronically activated HPAA in female patients [36], peripheral gonadotropin resistance in combination with abnormal central regulation stimulates increased pituitary follicle-stimulating hormone (FSH) secretion [37]. This evidence concerns the gene BRD2 and myeloid sarcoma.