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A persistent stimulation of endometriotic tissues with TGF-β1 was able to reduce NR4A1 activity through AKT-dependent phosphorylation, promoting fibrogenesis in OMA [34] and the treatment with Csn-B, an NR4A1 agonist, markedly decreased the expression of fibrotic markers in vitro and inhibited fibrogenesis in urine endometriosis models, suggesting a new potential target for the treatment of this disease [34]