KDM2B supports the EMT as elicited by TGF-β signaling upon repressing epithelial genes such as CDH1, which act in concert with PRC1/PRC2,231 whereas KDM1A interacts with SNAI1 to drive EMT-like programs in AML, promoting self-renewal and leukemogenesis.75 Notably, in breast cancer, cellular plasticity is facilitated by a bivalent chromatin state at the ZEB1 promoter in non-CSCs, which allows rapid EMT induction and transition into the CSC state in response to microenvironmental cues such as TGF-β.232. Here, KDM1A is linked to acute myeloid leukemia.