Primordial follicles maintain dormancy in the ovary and only a small number of them are activated towards ovulation every day. Several signaling pathways in oocytes and the surrounding flattened pre-granulosa cells have been shown to play crucial roles in primordial follicle activations and sex steroid hormones are also known to affect it. Intrinsic estrogen, estradiol, has been reported to suppress primordial follicle formation and the later primordial follicle activation in rodent neonatal ovaries. Conversely, some phytoestrogens and endocrine disruptors which possess intrinsic estrogen-like biological activity with different binding affinities to estrogen receptors, can activate primordial follicles. Testosterone and dehydroepiandrosterone have been used in fertility treatments in the expectation that they would activate primordial follicle, although evidence of their efficacy is inconclusive. Progesterone suppresses primordial follicle formation and the later primordial follicle activation in rodent neonatal ovaries. Synthetic progestins possess the ability to bind to steroid hormone receptors other than the progesterone receptor. Thus, progestins may regulate primordial follicle activation through other sex hormone receptors. It may be possible to regulate primordial follicle activation by sex steroid hormones in the future. However, it is not yet clear which pathway mediates the effect of these hormones on primordial follicle activation, and this will need to be studied in the future.