These findings demonstrated that the MEK/ERK pathway that relies on MAPK kinase acts as a sensitizer of endometrial cell proliferation and upregulates the expression of NF-κB, which promotes the proliferation and invasion of endometrial stromal cells, revealing that the MEK/ERK pathway is a potential target for the treatment of EMs. The gene discussed is NFKB1; the disease is eosinophilia-myalgia syndrome.