The molecular mechanisms involved in the endometriosis are not fully understood; however, there is evidence that leptin (LEP) and its receptor (LEPR) levels are significantly elevated in the peritoneal fluid of patients with endometriosis, suggesting that this hormone may be associated with the pathogenesis of the disease.(1-3) In addition, elevated levels of this hormone may activate signaling pathways that induce proliferation, inflammation, and angiogenesis, which are fundamental and well-known features of endometriosis and its painful symptoms.(2). Here, LEPR is linked to endometriosis.