Melatonin (MLT) paradoxically enhances metastatic progression in ovarian carcinoma through NE/AKT/β-catenin/SLUG axis potentiation, yet concurrently attenuates chemotherapy-related sequelae (CRS)-driven oncogenesis via SLUG-mediated epithelial-mesenchymal transition (EMT) suppression in preclinical models (Bu et al., 2020). This evidence concerns the gene SNAI2 and ovarian carcinoma.