This leads to a bold hypothesis: in addition to alleviating symptoms through the classic anti-inflammatory pathway, the eight NSAIDs widely used to treat endometriosis may also inadvertently promote cell migration and angiogenesis related to disease progression by activating EPHB4—a risk gene—and its downstream pathways, thereby potentially exacerbating the disease’s pathological process. Here, EPHB4 is linked to endometriosis.