On the basis of these observations, one may tenably argue that TGF-β1 is not a double-edged, molecular Jekyll and Hyde of cancer [135] which, anti-mitotic and pro-apoptotic in early neoplasia, morphs into a potent cancer driver at later stages of tumorigenesis; what happens in molecular terms is that the cytokine is used via the intermediacy of CAFs by the devious cancer cells to foster their growth and invasive program. Here, TGFB1 is linked to neoplasm.