PRMT4 was found to be indispensable to the onset of MLL-AF9-driven AML.412 PRMT4 could also negatively regulate CBP/p300 coactivation by methylating CBP.413 PRMT5 stimulated the self-renewal and viability of LSCs by triggering the Wnt/β-catenin pathway in CML.414 PRMT7 was shown to regulate glycine metabolism to preserve LSCs in CML, and the loss of PRMT7 downregulated glycine decarboxylase and propelled glycine metabolism to produce toxic methylglyoxal in LSCs without influencing normal hematopoiesis. The gene discussed is KMT2A; the disease is acute myeloid leukemia.