Notably, endometrial stromal β-catenin is required for steroid-dependent mesenchymal–epithelial crosstalk and decidualization [33]; whether the LPAR3/β-catenin pathway also contributes to the EMT processes in endometriosis and its possible crosstalk with the miR200/MALAT1 sponge requires further research. This evidence concerns the gene MALAT1 and endometriosis.