Consistent with a significant input of monocytes to LpM in endometriosis, our most striking result was revealed by constitutively limiting monocyte recruitment (using both Ccr2−/− and Ccl2−/− mice) and subsequently reducing both LpM and SpM replenishment, which resulted in mice with induced endometriosis developing significantly more lesions. The gene discussed is CCR2; the disease is endometriosis.