To determine the potential causal role of FTO-mediated m6A regulation in the development of endometriosis in vivo, we generated mice with uterine deletion of Fto (Ftod/d) by injecting Fto floxed C57BL/6 J mice (Ftof/f) with Cre-AVV through the uterus (Fig. 3A). The gene discussed is FTO; the disease is endometriosis.