Over-activation of signalling pathways such as Wnt/β-catenin, TGFβ, mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and nuclear factor kappa B (NF-κB) has been widely reported to contribute to cancer cell survival and the acquisition of a meta-static phenotype[87]. This evidence concerns the gene TGFB1 and cancer.