Tumor cells with EGFR amplification [9], those in the process of migration or exposed to hypoxia [7,8] all have been shown to express higher levels of ZEB1 than controls and experimental studies have identified molecular mechanisms involved in ZEB1 regulation, such as PDGFRA, Wnt- or TGF-beta signaling [6,35–37]. This evidence concerns the gene ZEB1 and neoplasm.