Recently, there have been two manuscripts delineating the role for ZEB1 in HSCs and their differentiation using models with Zeb1−/−, where there was an acceleration of MLL-AF9 and Meis1a/Hoxa9-driven AML progression, implicating Zeb1 as a tumor suppressor in AML LSCs [52]. The gene discussed is KMT2A; the disease is neoplasm.