HGF, produced and released into tumor microenvironment by both ASCs and breast cancer cells, could have a dual role: on the one hand, it could favor recruitment of several cell types to tumor sites, on the other hand, acting as a transforming factor for c-Met expressing breast cancer cells, could exacerbate tumor phenotype by stimulation of migratory activity and acquisition of a metastatic signature, giving tumor a chance to spread in different tissues. This evidence concerns the gene MET and breast carcinoma.