Fig. 1

PRMT7 seizes glycine metabolism switch to determine fate of LSCs. A PRMT7 catalyzes H2AR3me2s to inhibit the transcription repressor of TRPS1, eventually upregulating GLDC in CML LSCs. Glycine generated from serine by SHMT2 is converted by GLDC to 5, 10-MTHF, allowing LSCs to gain metabolic addiction. B Genetic deletion or pharmacological inhibition of PRMT7 derepresses the repressor TRPS1, thereby downregulates GLDC and subsequently accumulates intracellular glycine in CML LSCs. Increased intracellular glycine is converted by GCAT to methylglyoxal, which induces the death of CML LSCs