Shi et al. [66] confirmed the role of Brg1/Smarca4 in the maintenance of proliferation and disease progression in mouse models of AML and ALL as well as in patient cell lines, where knockdown of Brg1/Smarca4 and other complex members led to a loss of proliferation, the induction of differentiation, downregulation of oncogenic transcription, particularly Myc and Hoxa9 gene signatures, and prolonged survival in vivo [66]. The gene discussed is SMARCA4; the disease is acute lymphoblastic leukemia.