On the other hand, increasing evidence shows that excess production and/or activation of TGF-β in tumors can accelerate cancer progression by a combination of autocrine and paracrine mechanisms, resulting in enhancement of tumor cell motility and survival, increase in tumor angiogenesis and production of extracellular matrix and peritumoral proteases, and the inhibition of immune surveillance mechanisms in the cancer host (reviewed in [34, 35, 45]). This evidence concerns the gene TGFB1 and neoplasm.