The results showed that the expression levels of MEK, ERK, and NF-κB proteins in the model and DMSO groups in the eutopic and ectopic endometrial tissues were significantly increased, indicating that the overexpression of MEK protein in EMs promotes the expression of ERK and downstream effector NF-κB, which leads to abnormal activation of the MEK/ERK and NF-κB pathways in the EMs rat model and promotes the growth of ectopic lesions, which is obviously related to the occurrence and development of EMs. Here, NFKB1 is linked to eosinophilia-myalgia syndrome.