Moreover, depending on the intensity and duration of oxidative, metabolic, and environmental stress, FOXO1 drives distinct cellular fates-including decidualization, senescence, and apoptosis-thus contributing to the persistence and progression of endometriotic lesions.<h4>Conclusion</h4>Dysregulation of the FOXO1-dependent cellular fate-control network plays a central role in the development of endometriosis. Here, FOXO1 is linked to endometriosis.