However, it should be consider that ASCs support breast cancer tumorigenesis through a well orchestrated mechanism involving different compartments of a pathological microenvironment [55], therefore combined therapies may reveal more effective to increase drug responsiveness of tumor cells [26, 27] as combining c-Met inhibitors with rapamycin treatment, blocking AKT-mediated cell proliferation, or with PI3K inhibitors impairing beta-catenin stabilization and tumor self-renewal, or with drugs specifically targeting signaling pathways sustaining CICs. The gene discussed is MET; the disease is neoplasm.