Given our previous data showing that TGF-β signaling leads to functional inhibition of GSK-3β activity through pAkt activation [23], it appears that Nodal expression may be regulated by both Smad- and non-Smad-dependent pathways in response to TGF-β action in the endometriosis-OCCCa lesions. The gene discussed is TGFB1; the disease is endometriosis.