ROS has been shown to mediate many effects of TGF-β in cancer progression, by deregulating tumor suppressors and, at the same time, by promoting tumorigenesis; one of the mechanisms of crosstalk between ROS and TGF-β in cancer cell metabolism shows ROS as directly involved in the regulation of the TGF-β pathway, thus involving factors such as SMAD, MAPK and NF-kB, and in turn promoters of cell proliferation and motility [55], particularly by increasing SMAD and thus making tumor cells resistant to the inhibition of proliferation exerted by TGF-β in the initial step of tumorigenesis [56]. This evidence concerns the gene TGFB1 and neoplasm.