Increased estradiol can play a role in antiinflammatory action via suppressing interferon and nuclear factor kappa B signaling.[30,31] Moreover, high levels of estradiol prefer to shift T helper cells toward the repair skewed Th2 transcription profile relating to IL-4 during pregnancy.[32] Therefore, we supposed that the shift of T helper cells toward the Th1 type as well as cytokines increasing during sudden deficiency of estradiol affected the development of mouth ulcers, and the T helper cells toward the Th2 type after estradiol being supplemented reversed the state. The gene discussed is IL4; the disease is Oral ulcer.