ZEB1 and neoplasm: This EMT-MET plasticity is part of a more extensive and complex CSC plasticity, through which CSCs and non-CSCs can be converted one in the other and vice versa [73], due to the action of key TFs; for example, a poised chromatin structure in the ZEB1 promoter allows non-CSCs to promptly adapt to changing microenvironmental cues, hence increasing their tumor-initiating ability [82].