These interplay of the different factors in the tumour microenvironment, including therapeutic pressures can also promote the induction of CSCs from non-CSCs, and seems to be mediated by common signalling pathways predominantly the Notch, NF-κB, TGF-β, Wnt/β-catenin, and MAPK signalling pathways, to name a few [29–31]. The gene discussed is TGFB1; the disease is neoplasm.