Conclusively, our study primarily demonstrates that disordered cholesterol metabolism and activated estrogen biosynthesis states exist in EMs lesions, and high local estrogen level derived from ectopic ESC induces augmented expression of PrPC, which serves as a critical mediator in encouraging cholesterol accumulation and estrogen production through negatively regulating PPARα pathway, ultimately promoting EMs progression (Figure 9). This evidence concerns the gene PRNP and eosinophilia-myalgia syndrome.