Several phenomena associated with tumor initiation, such as inflammation [42], physical constrains (including hydrostatic pressure, shear stress and tension forces) [43], abnormal activation of signaling pathways such as those controlled by WNT, NOTCH, or TGFβ [4], [44], and hyperactivation or RAS-ERK1/2 signaling [45] are known to trigger expression of EMT-promoting factors and could thus induce reactivation of these embryonic transcription factors in early stages of tumor development, as previously observed in animal models [46]. The gene discussed is TGFB1; the disease is neoplasm.