The proposed mechanism of PRP's action on breast tumor cells is that: 1) PRP provides the best growth factors to proliferated breast tumor cells (including TGF-β); 2) PRP mimics the network of fibrin bundles present in the breast cancer environment promoting the selection of cells with the highest potential for malignancy, activating the EMT process, and enhancing proteolytic activity; 3) PRP induces alterations in the focal adhesion complex that contributes to EMT; and 4) PRP efficiently induces endothelial cell type formation in co-cultures with breast tumor cells and HUVEC. This evidence concerns the gene TGFB1 and breast carcinoma.