Molecular studies of endometriosis have reported significant findings based on the Wnt-B-catenin signaling pathway and its relationship with the levels of vascular endothelial growth factor (VEGF) and E2, whose association triggers decreased levels of GSK3β and E-cadherin and increased levels of nuclear β-catenin in endometriotic lesions when compared with uterine endometrial tissue. This evidence concerns the gene GSK3B and endometriosis.