Moreover, in lesions recovered from Ccr2−/− and Ccl2−/− mice we could still detect monocytes using immunodetection (Figs. 4 H and I and 5 G and H), indicating that there is redundancy in the CCL2–CCR2 axis in the presence of endometriosis lesions and suggesting that monocytes may also be recruited via another mechanism. This evidence concerns the gene CCR2 and endometriosis.