In view of the fact that fibrosis is a characteristic feature of endometriosis and the expression of ILK in renal tubular epithelial cells is strictly controlled by TGF-β1 and dependent on intracellular SMAD signaling [46,72], we speculate that an analogous molecular mechanism could occur in endometrial epithelial cells and promote their mesenchymal transformation in endometriosis. The gene discussed is TGFB1; the disease is endometriosis.