Therefore, the level of Ki-67 in MRC2-silenced ESCs increased compared with that in the vector group (Figures 5e and f), which is consistent with the notion that ectopic ESCs have a stronger ability for proliferation.6 Similarly, the expression of Ki-67 and IDO1 also increased in ectopic lesions after MRC2 shRNA was intraperitoneal injected to the peritoneal cavity of endometriosis mice model in vivo (Figures 5h and i). Here, MKI67 is linked to endometriosis.