Hypoxia, an hallmark of endometriosis, induces CXCL12 expression.58 Similarly, aberrant oestrogen signalling and progesterone resistance further amplified CXCL12‐CXCR4 axis activation in endometrial cells and endometriosis.45, 46 Targeting CXCR4 or CXCR7 using AMD3100 or CCX771, respectively, in this preclinical model of endometriosis was effective in preventing and treating ectopic lesions by affecting BM cell engraftment. Here, ACKR3 is linked to endometriosis.