The presence of shared somatic mutations between endometriotic lesions and OEC—such as AT-rich interaction domain 1A (ARID1A) loss-of-function and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) gain-of-function mutations—supports the hypothesis that OEC may arise from endometriosis [26,27]. Here, PIK3CA is linked to endometriosis.