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]. The gene discussed is NR4A1; the disease is endometriosis.