Interestingly, ESCendo express CXCR4 and may hence be recruited to ectopic lesions by CXCL12, which may also possess nonimmune functions in endometriosis, such as promotion of tissue repair, angiogenesis, migration, invasion, and suppression of apoptosis [1, 38, 39], processes proposed to be involved in growth of ectopic lesions. Here, CXCL12 is linked to endometriosis.